“METHODS FOR ASSESSING COMPLIANCE OR NON-COMPLIANCE OF TREATMENT AND CHRONIC MYELOID LEUKEMIA PROGRESSION OR NON- PROGRESSION” TECHNICAL FIELD The present disclosure pertains to the field of molecular oncology/biotechnology. The present disclosure relates to a method of assessing compliance or non-compliance of tyrosine kinase inhibitors (TKI) treatment and determining progression or non-progression of CML in a subject. In particular, the present disclosure allows for biomarkers for the identification of patients which are TKI compliant and its correlation with disease progression. The present disclosure also relates to a combination of at least two or more biological markers employed in the method for evaluation of TKI compliance and/or disease progression in CML patients and assays, kits for said evaluation. BACKGROUND OF THE DISCLOSURE Chronic Myeloid leukemia (CML) is a clonal expansion of the myeloid hematopoietic cells. It is associated with a reciprocal translocation between Chromosome 9 and 22 leading to the formation of a shortened 22nd chromosome – called Philadelphia chromosome. This translocation leads to the fusion of 2 genes: BCR and ABL1 which is the hallmark of CML and leads to constitutive activation of ABL, a tyrosine kinase. CML has three clinical stages. It starts as a chronic phase (CP), often asymptomatic, followed by the accelerated phase (AP) with an increase in the Leukemia stem cells (LSCs; CD34+BCR-ABL+ cells). The blast crisis (BC) stage is marked by the further increase in LSCs. In 1970s, CML was treated using alkylating agent such as busulfan or hydroxyurea. Neither therapy prevented the progression of disease from CP to AP/BC stages. This paved way for interferon alpha (INFA) therapy in 1980s which was able to induce a cytogenetic response. Breakthrough came in the 1990s when a small molecule Signal Transduction Inhibitor 571 (STI571), a tyrosine kinase inhibitor (TKI) was identifieed that could inhibit the constitutively active tyrosine kinase produced by the fusion of BCR-ABL1. Since 2001, this drug now known as Imatinib (marketed as Glivec®/ Gleevac), has changed the landscape of CML. Today, CML is one of the rare cancers where, a highly effective but a life-long targeted monotherapy using TKI-drugs is available. Currently, Imatinib is used as the First line of treatment and can maintain most CP patients with normal life expectancy. Successful long-term management of CML patients on TKI- monotherapy has also encouraged treatment discontinuation studies e.g. The Stop Imatinib (STIM) study. However, the results are not completely encouraging. Patients on Imatinib for at least 50- months with complete molecular response (CMR) were considered for Imatinib discontinuation and closely monitored for at least 12-months.The molecular relapse-free survival was only 41% at 12-months, which was further reduced to 38% at 24-months (Mahon et al., 2010). Thus, currently stopping imatinib is still not recommended without close monitoring and indefinite-therapy remains the standard of care. In India, CML accounts for 30-60% of all adult leukemias. Data collected across different centers in India suggests that the age of presentation of CML in India is at least a decade younger (32- 42years) compared to Europe (55 years) or America (66 years) (Bansal et al., 2013; Singhal et al., 2016; Yanamandra et al., 2018). Hence achieving treatment-free remission in Indian patients is most desirable. Indian retrospective observational clinical data from 1950-patients suggests that ~80% of CML patients undergo complete cytogenetic response (CCyR), and major molecular response (MMR) is found in 84.5% of patients. However, loss of CCyR and MMR is observed in ~37.2% and 28.4% respectively (Yanamandra et al., 2018). A 7-year update of CML patients on Imatinib suggested that only 57% of patients were in continuing CMR (Singhal et al., 2016). A study from Jaipur suggests that 73% of Indian progressive patients do not have the known mutation in the TKI drug binding site (i.e., T315I or M351T) (Bansal et al., 2013). No correlation is identified between the expression of drug-transporters in Indian patients and Imatinib response (Malhotra et al., 2015). It is rather acknowledged that the requisite indefinite therapeutic regime of TKI has introduced a new challenge of therapy non-compliance (Menon, 2017; Yanamandra et al., 2017). Clinical studies across time have recommended that adherence to Imatinib is necessary to achieve and maintain MMR. Discontinuation of TKI-monotherapy, due to toxicity or non- compliance, often leads to rapidly progressive disease. Clinical observational studies suggest that one-third of Indian CML patients are non-compliant. Such patients often develop progressive disease and demonstrate an inferior response if resumed on TKI-therapy. The only way to help here is by bone marrow transplant which has its own limitations and challenges including the socioeconomic challenge. Overall, it is important for clinics to identify TKI-noncompliance before it is too late to intervene, to further improve outcomes in this disease. However, estimating non-compliance to prescribed drugs is often challenging in clinics. Keeping in mind that patients in India at the time of diagnosis are symptomatic (in contrast to the Western counterparts) as well as present in Intermediate sokal risk category, it is important to also be able to stratify patients with greater likelihood of disease advancement/progression. The present disclosure primarily addresses this clinical need. The inventors of the present invention have identified that it is possible to use molecular markers to gauge the compliance and progression of the CML. The inventors have for the first time developed a method to correlate the expression of NFkB pathway genes, Apoptosis pathway genes and Ion channels genes in presence of Imatinib in CML to make an assessment over the treatment compliance and disease progression. Object of the present invention Accordingly, the present disclosure identifies one or more progressive biomarkers which can be employed for assessing disease progression before BCR-ABL status changes and two or more TKI compliance biomarkers which can be employed for assessing TKI compliance or non-compliance in patients suffering from CML. Therefore, an object of the present invention provides a method for determining TKI compliance or non-compliance in a patient suffering from CML, and/or for evaluating progression or regression of pathology in the said CML patient. An object of the present invention provides a method for determining the activity, the stage, or the severity of CML in a subject, and/or for classifying a subject as a potential receiver or non-receiver of treatment for CML. An object of the present invention provides a method for classifying a subject for starting, continuing or stopping a specific course of treatment for CML, particularly a treatment with one or more TKI. An object of the present invention provides a method for classifying a patient as a potential responder or non-responder to a medical treatment comprising TKI. An object of the present invention provides a method for predicting or prognosing disease outcome for a CML patient, in relation to compliance or non-compliance to a TKI treatment. An object of the present invention provides a computer-implemented method for assessing compliance or non-compliance of tyrosine kinase inhibitors (TKI) treatment and determining progression or non-progression of CML in a subject. An object of the present invention provides an assay system for compliance or non-compliance of TKI treatment and determining progression or non-progression of CML in a subject. An object of the present invention provides a kit for assessing compliance or non-compliance of tyrosine kinase inhibitors (TKI) treatment and determining progression or non-progression of CML in a subject. Summary of Invention The present disclosure relates to identification of biologicals markers in a CML patient for evaluating the efficacy of a treatment being administered to the said patient. The present disclosure relates to correlating Nuclear Factor kappa-light chain-enhancer of activated B-cells (NF-kB)- signalling pathway, Sonic-hedgehog (Shh) pathway and targets, apoptotic pathways and voltage- gated ion channels expressions etc. in patients suffering from CML to disease progression and/or TKI treatment compliance by the patients. Accordingly, the present invention provides a method of assessing compliance or non- compliance of tyrosine kinase inhibitors (TKI) treatment and determining progression or non- progression of CML in a subject, wherein the method comprises assessing the expression of a combination of one or more progressive marker and two or more TKI compliance markers. Furthermore, the present disclosure also relates to assays, kits and computer implemented methods for the said identification of the biological biomarkers and their use in the assessment of TKI treatment compliance and disease progression. BRIEF DESCRIPTION OF THE ACCOMPANYING FIGURES The accompanying drawings illustrate some of the embodiments of the present disclosure and, together with the descriptions, serve to explain the disclosure. These drawings have been provided by way of illustration and not by way of limitation. The components in the drawings are not necessarily drawn to scale, emphasis instead being placed upon clearly illustrating the principles of the aspects of the embodiments. Figure 1: RNA-SEQ analysis to identify Differentially expressed Genes (DEGs). A) Density plot of the DEGs in 4 cell lines (K562, K562_SHH, K562 with Imatinib and K562 with Shh+Imatinib+. B) Volcano plot of the distribution of all DEGs with SHH+, IMAT+ and SHH+IMAT+ with respect to the control (K562) mapping the up-regulated (red) and down- regulated (blue) genes. C) Heat map of the up and down regulated DEGs under Shh+Imat+ condition. D) Functional enrichment of DEGs in i. K562 with Imatinib and ii. K562 with Shh+Imat+. Figure 2: NF-kB pathway genes are inhibited by Imatinib. A). Heat map of NF-kB signalling pathway genes identified using pathway prediction approach after identification of DEGs across samples using RNA-seq data of 4 cell lines (K562, Shh-K562, K562+Imatinib and Shh-K562+Imatinib and in B-C) Heat map of NF-kB-signalling genes from CP (at diagnosis) and Progressive CML-patients (AP/BC), B). with and without drug-binding site mutation (EGAD00001004179). C). Matched samples collected at diagnosis (before Imatinib) and at disease progression (after prescribing Imatinib). Figure 3: Pro-apoptotic genes and ion-channels are down regulated by Imatinib Heat map of A) pro-apoptotic genes (from KEGG) and B) Voltage-gated ion channel signalling pathway in CP and AP/BC (progressive) - CML patients with and without BCR-ABL1+ domain site mutation (EGAD00001004179). C) Violin plots for selected pro-apoptotic genes in CP (A) and AP/BC (progressive) (B) - CML patients with and without BCR-ABL1+ domain site mutation (EGAD00001004179). Figure 4: Shh-pathway is up-regulated in Progressive CML patients. A). Heat map showing expression of Shh-pathway genes (from KEGG) using RNAseq data i. (EGAD00001004179) of CP and Progressive (BC) - CML patients with and without BCR-ABL1+ domain site mutation and ii. (GSE33075) CP patients at diagnosis and 1 month post Imatinib treatment. B) Violin plots of selected genes from the SHH pathway in CP and progressive (BC) – CML patients with and without BCRABL1+ domain site mutation from the RNA-seq data (EGAD00001004179) . C) Heatmap of matched samples for selected Shh genes using RNA-seq data from EGAD00001004179. Figure 5: QPCR validation of select molecular markers identified by RNAseq to report non- compliance: A. CML cells (K562) were treated with imatinib for 3days (pink bars, A) or 6 days (red bars, A), Imatinib was washed off after 3days of treatment and relative gene-expression was examined after 3 days of additional culture (White bars, A). B. Other human cell lines namely, Sup-B15, B-ALL cell-line with same causative mutation (BCR- ABL; grey bars, B) and HEK-293T cells without the causative mutation (black bars, B) were used as controls, treated with imatinib for 3days. The gene expression is normalized to respective untreated cells for each gene, represented as dotted reference line in A & B. Suppression of FAS, BID is specific to BCR-ABL cell-lines not applicable to human cells without BCR-ABL translocation HEK cells (compare difference from dotted line). RelA, IRAK1, and CASP9 suppression is highly specific to CML cell-line. HEK-293T cells (black bars, B) do not show suppression of any genes upon imatinib treatment. DETAILED DESCRIPTION OF THE DISCLOSURE The present disclosure is now described with reference to the tables/figures and specific embodiments, including the best mode contemplated by the inventors for carrying out the disclosure. This description is not meant to be construed in a limiting sense, as various alternate embodiments of the disclosure will become apparent to persons skilled in the art, upon reference to the description of the disclosure. It is therefore contemplated that such alternative embodiments form part of the present disclosure. Unless defined otherwise, technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this disclosure belongs. Further, unless otherwise required by context, singular terms shall include pluralities and plural terms shall include the singular. Generally, nomenclatures used in connection with, and techniques of biotechnology, molecular oncology, molecular and cellular biology described herein are those well-known and commonly used in the art. Certain references and other documents cited herein are expressly incorporated herein by reference. In case of conflict, the present specification, including definitions, will control. The materials, methods, figures and examples are illustrative only and not intended to be limiting. Before the method of evaluating TKI compliance, biomarkers, kit comprising antibodies, primers or probes against said markers and other embodiments of the present disclosure are disclosed and described, it is to be understood that the terminologies used herein are for the purpose of describing particular embodiments only and are not intended to be limiting. It must be noted that, as used in the specification and the appended claims, the singular forms “a,” “an” and “the” include plural referents unless the context clearly dictates otherwise. As used herein, “tumor” or “cancer” are terms as well known in the art and used interchangeably throughout the disclosure. “Marker” or “biomarker” or “molecular marker” means an entire gene, or an EST derived from that gene, the expression or level of which changes between certain conditions. Where the expression of the gene correlates with a certain condition, the gene is a marker for that condition. The term “marker” in the present disclosure relates to predicting disease progression or treatment compliance with respect to any specific therapy/treatment/drug. The term “Chronic Myeloid Leukemia” (CML) in the present disclosure refers to a type of cancer that affects the blood and bone marrow. The term "biomarker panel," "biomarker profile," or "biomarker fingerprint" refers to a set of biomarkers. As used herein, these terms can also refer to any form of the biomarker that is measured. Thus, if NEFL is part of a biomarker panel, then either NEFL mRNA, for example, or protein, for example, could be considered to be part of the panel. While individual biomarkers are useful as diagnostics, combination of biomarkers can sometimes provide greater value in determining a particular status than single biomarkers alone. Specifically, the detection of a plurality of biomarkers in a sample can increase the sensitivity and/or specificity of the test. The term "assay system" defines means for detecting a desired activity which is encapsulated within a screening unit. An assay system directly or indirectly produces a detectable and/or measurable signal when it contacts or reacts with a biomarker or biomarker panel of the present invention. The assay system used herein is a PCR-based assay system or an immunoassay system. The term "in vitro method" refers to a biochemical process performed in a test tube or other laboratory instrument. The term implies that said method is carried out in a biological sample isolated from the subject from whom it is taken. The term “diagnosis,” as used herein, refers to the determination of a condition of a subject, such as determining whether the subject has a particularly disease condition, susceptibility, or other trait. The term “prognosis” in the present disclosure relates to predicting disease progression 35 without considering any reference to therapy/treatment/drug. Quantitative or qualitative way of prognosis includes age, genetic risks, expression levels of the various neuropathological biomarker, psychometric testing, neuroimaging, etc. Prognosis is done to prognosis relates to understanding the long-term outcome of a disease. Before the biomarker panels, assay systems, methods of diagnosis/prognosis, kits comprising reagents for detection of the biomarkers, and other embodiments of the present disclosure are disclosed and described; it is to be understood that the terminologies used herein are to describe particular embodiments only and are not intended to be limiting. The present disclosure relates to identification of treatment compliance and/or non- compliance and disease progression using molecular markers. The present disclosure has, for the first time, identified specific combination(s) of genes/biomarkers, whose expression together can make it clinically feasible to discern which patient is in need of more attention. The present disclosure therefore primarily relates to a method for determining TKI compliance by a patient suffering from CML, and/or for evaluating progression or regression of pathology in the said CML patient. The present disclosure also relates to a method for determining the activity, the stage, or the severity of CML in a subject, and/or for classifying a subject as a potential receiver or non-receiver of treatment for CML. While the TKI exemplified in the context of the present disclosure is Imatinib (marketed as Glivec®/ Gleevac), a person skilled in the art would be able to perform the methods of the present disclosure for any other TKI as well. Particularly, the present disclosure relates to identification of biomarkers in a CML patient for evaluating the efficacy of a treatment being administered to the said patient. Furthermore, the present disclosure also relates to kits for the said identification and evaluation. The present disclosure also relates to correlating involvement of Nuclear Factor kappa- light chain-enhancer of activated B-cells (NF-kB)-signalling pathway, Sonic-hedgehog (Shh) pathway and target genes, apoptotic pathways and voltage-gated ion channels expressions in patients suffering from CML to disease progression and/or TKI treatment compliance by the patients. Accordingly, an important embodiment of the present invention provides a method of assessing compliance or non-compliance of tyrosine kinase inhibitors (TKI) treatment and determining progression or non-progression of CML in a subject, wherein the method comprises assessing the expression of a combination of one or more progressive marker and two or more TKI compliance markers, the method comprising the steps: a. obtaining a biological sample taken from a subject undergoing treatment with tyrosine kinase inhibitors (TKI), b. preparing single stranded cDNA from cellular RNA by a reverse transcription (RT) reaction comprising (1) denaturing the cellular RNA; (2) annealing one or more primers to the cellular RNA; and (3) extending the cellular RNA- primer moiety to form the single stranded cDNA; (4) fragmenting the single stranded cDNA into smaller strands; wherein the sequences of cellular RNA consist of RNA sequences from the one or more cells; c. contacting the smaller cDNA strands with the primer set that are each specific for a respective biomarker present on the cDNA; d. amplification of the cDNA through PCR and feeding the amplified product to high- throughput sequencing machines for quantifying binding of the primer to the respective progressive and TKI compliance biomarker in order to measure expression of two or more biomarkers and e. obtaining statistical score based on measuring the expression of combination of two or more TKI compliance biomarkers to assess the TKI treatment compliance or non- compliance and wherein the upregulation of one or more progressive biomarkers is indicative of the gradual progression or non-progression of the CML. An embodiment of the present invention provides the method, wherein the upregulation of the two or more TKI compliance biomarkers are indicative of TKI treatment non-compliance. An embodiment of the present invention provides the method wherein the progressive biomarkers are from the genes activated by the SHH pathway and are selected from but not limited to Shh, Gli-1, Smo, BCL-2, CD-34 and CCND-2, and/or any combination thereof. An embodiment of the present invention provides the method, wherein TKI compliance biomarkers are genes from the apoptotic pathways and are selected from but not limited to RELA, FADD, BID, CASP9, IRAK1, FAS and BAD, or any combination thereof. An embodiment of the present invention provides the method, wherein one or more primer set complimentary to the biomarkers selected from but not limited to SEQ ID No.1 and SEQ ID No. 2 wherein the primer set is specific to GAPDH, SEQ ID No.3 and SEQ ID No. 4 wherein the primer set is specific to Beta-Actin, SEQ ID No.5 and SEQ ID No. 6 wherein the primer set is specific to Sonic Hedgehog, SEQ ID No.7 and SEQ ID No. 8 wherein the primer set is specific to Bcl2, SEQ ID No.9 and SEQ ID No. 10 wherein the primer set is specific to Gli-1, SEQ ID No.11 and SEQ ID No. 12 wherein the primer set is specific to REL A, SEQ ID No.13 and SEQ ID No. 14 wherein the primer set is specific to FAS, SEQ ID No.15 and SEQ ID No.16 wherein the primer set is specific to BID, SEQ ID No.17 and SEQ ID No. 18 wherein the primer set is specific to REL, SEQ ID No.19 and SEQ ID No. 20 wherein the primer set is specific to RELB, SEQ ID No.21 and SEQ ID No. 22 wherein the primer set is specific to IRAK1, and SEQ ID No.23 and SEQ ID No. 24 wherein the primer set is specific to CASP9. An embodiment of the present invention provides the method, wherein the statistical score is calculated through the formula: ^ = ^{×ି^} ఙ Wherein z = Z Score, provides probability scores for up-regulation in gene expression x = gene expression (gene-of-interest) in samples from CML patients X = median of gene expression in healthy subjects, σ = standard deviation of gene expression in healthy subjects and wherein the probability of the up regulation in at least any or all genes in Progressive biomarkers and/or at least two TKI-compliance biomarkers each is at least 60%. An embodiment of the present invention provides the method as claimed in 1, wherein the method is performed in vitro. Yet another important embodiment of the present invention provides an in vitro method for predicting or prognosing disease outcome for a CML patient, for determining the activity, the stage, or the severity of CML in a subject, and/or for classifying a subject as a potential receiver or non-receiver of treatment for CML, wherein the method comprises: a. obtaining a biological sample taken from a subject undergoing treatment with tyrosine kinase inhibitors (TKI), b. contacting the biological sample with primer sets that are each specific for a respective biomarker; wherein the primer sets are selected from but not limited to SEQ ID No.1 and SEQ ID No. 2 wherein the primer set is specific to GAPDH, SEQ ID No.3 and SEQ ID No. 4 wherein the primer set is specific to Beta-Actin, SEQ ID No.5 and SEQ ID No.6 wherein the primer set is specific to Sonic Hedgehog, SEQ ID No.7 and SEQ ID No. 8 wherein the primer set is specific to Bcl2, SEQ ID No.9 and SEQ ID No. 10 wherein the primer set is specific to Gli-1, SEQ ID No.11 and SEQ ID No. 12 wherein the primer set is specific to REL A, SEQ ID No.13 and SEQ ID No. 14 wherein the primer set is specific to FAS, SEQ ID No.15 and SEQ ID No.16 wherein the primer set is specific to BID, SEQ ID No.17 and SEQ ID No. 18 wherein the primer set is specific to REL, SEQ ID No.19 and SEQ ID No. 20 wherein the primer set is specific to RELB, SEQ ID No.21 and SEQ ID No. 22 wherein the primer set is specific to IRAK1, and SEQ ID No.23 and SEQ ID No. 24 wherein the primer set is specific to CASP9; c. quantifying binding of each primer to the respective biomarker in order to measure expression of two or more progressive biomarkers and two or more TKI compliance biomarkers through quantitative polymerase chain reaction and d. obtaining measurements of upregulation of the combination of two or more progressive biomarkers and two or more TKI compliance biomarkers to assess the disease outcome for a CML patient for determining the activity, the stage, or the severity of CML in a subject, and/or for classifying a subject as a potential receiver or non-receiver of treatment for CML. An embodiment of the present invention provides the method, wherein the progressive biomarkers are from the genes activated by the SHH pathway and are selected from but not limited to Shh, Gli-1, Smo, BCL-2, CD-34 and CCND-2, and/or any combination thereof and the TKI compliance biomarkers are genes from the NfkB and apoptotic pathways and are selected from but not limited to RELA, FADD, BID, CASP9, IRAK1, FAS and BAD, or any combination thereof. Yet another embodiment of the present invention provides an in vitro method wherein the method comprises measuring expression of at least two gene or biomarkers by assaying a biological sample with a one or more primer sets selected from but not limited to SEQ ID No.1 and SEQ ID No. 2 wherein the primer set is specific to GAPDH, SEQ ID No.3 and SEQ ID No. 4 wherein the primer set is specific to Beta-Actin, SEQ ID No.5 and SEQ ID No. 6 wherein the primer set is specific to Sonic Hedgehog, SEQ ID No.7 and SEQ ID No. 8 wherein the primer set is specific to Bcl2, SEQ ID No.9 and SEQ ID No. 10 wherein the primer set is specific to Gli-1, SEQ ID No.11 and SEQ ID No. 12 wherein the primer set is specific to REL A, SEQ ID No.13 and SEQ ID No. 14 wherein the primer set is specific to FAS, SEQ ID No.15 and SEQ ID No.16 wherein the primer set is specific to BID, SEQ ID No.17 and SEQ ID No. 18 wherein the primer set is specific to REL, SEQ ID No.19 and SEQ ID No. 20 wherein the primer set is specific to RELB, SEQ ID No.21 and SEQ ID No. 22 wherein the primer set is specific to IRAK1, and SEQ ID No.23 and SEQ ID No. 24 wherein the primer set is specific to CASP9. Yet another important embodiment of the present invention provides an assay system for compliance or non-compliance of TKI treatment and determining progression or non-progression of CML in a subject, said system comprising: a. a plurality of primer sets for amplifying a biomarker panel wherein primer set are selected from but not limited to SEQ ID No.1 and SEQ ID No. 2 wherein the primer set is specific to GAPDH, SEQ ID No.3 and SEQ ID No. 4 wherein the primer set is specific to Beta-Actin, SEQ ID No. 5 and SEQ ID No. 6 wherein the primer set is specific to Sonic Hedgehog, SEQ ID No.7 and SEQ ID No. 8 wherein the primer set is specific to Bcl2, SEQ ID No.9 and SEQ ID No. 10 wherein the primer set is specific to Gli-1, SEQ ID No.11 and SEQ ID No. 12 wherein the primer set is specific to REL A, SEQ ID No.13 and SEQ ID No. 14 wherein the primer set is specific to FAS, SEQ ID No.15 and SEQ ID No.16 wherein the primer set is specific to BID, SEQ ID No.17 and SEQ ID No. 18 wherein the primer set is specific to REL, SEQ ID No.19 and SEQ ID No. 20 wherein the primer set is specific to RELB, SEQ ID No. 21 and SEQ ID No. 22 wherein the primer set is specific to IRAK1, and SEQ ID No.23 and SEQ ID No. 24 wherein the primer set is specific to CASP9, b. means to measure the expression levels of the gene expression of step (a) through PCR- based assay systems; and c. a processing unit configured to estimate the upregulation or downregulation of one or more progressive or TKI compliance biomarkers to statistically calculate a score for assessment of compliance or non-compliance of TKI treatment and determining progression or non-progression of CML in a subject. Yet another important embodiment of the present invention provides a computer- implemented method for assessing compliance or non-compliance of tyrosine kinase inhibitors (TKI) treatment and determining progression or non-progression of CML in a subject, said method comprising: a. receiving, by a processing unit of an assay system as claimed in claim 8, expression levels of progressive biomarkers selected from a group comprising to Shh, Gli-1, Smo, BCL-2, CD-34 and CCND-2 and/or any combination thereof and at least two or more TKI compliance biomarkers selected from a group comprising RELA, FADD, BID, CASP9, FAS, IRAK1 and BAD, and/or any combination thereof, wherein the expression levels are measured using high through put sequencing systems; b. determining, by the processing unit, a score associated with the received expression levels of biomarkers by the formula: ^ = ^{×ି^} ఙ Wherein z = Z Score, provide probability scores for up-regulation in gene expression x = gene expression in samples from CML patients X = median of gene expression in healthy subjects, σ = standard deviation of gene expression in healthy subjects c. estimating, by the processing unit, the progression of the disease and/or TKI treatment compliance based on the risk score thus determined. Yet another important embodiment of the present invention provides a kit for assessing compliance or non-compliance of tyrosine kinase inhibitors (TKI) treatment and determining progression or non-progression of CML in a subject, wherein the kit comprises: buffers, reagents, solvents for RNA extraction from the cells in a biological sample, primer sets for preparing the cDNA library targeting two or more gene progressive and TKI compliance biomarkers, wherein the primers and probes are selected from but limited to SEQ ID No. 1 and SEQ ID No. 2 wherein the primer set is specific to GAPDH, SEQ ID No.3 and SEQ ID No. 4 wherein the primer set is specific to Beta-Actin, SEQ ID No.5 and SEQ ID No. 6 wherein the primer set is specific to Sonic Hedgehog, SEQ ID No.7 and SEQ ID No. 8 wherein the primer set is specific to Bcl2, SEQ ID No.9 and SEQ ID No. 10 wherein the primer set is specific to Gli-1, SEQ ID No.11 and SEQ ID No. 12 wherein the primer set is specific to REL A, SEQ ID No.13 and SEQ ID No. 14 wherein the primer set is specific to FAS, SEQ ID No.15 and SEQ ID No.16 wherein the primer set is specific to BID, SEQ ID No.17 and SEQ ID No. 18 wherein the primer set is specific to REL, SEQ ID No.19 and SEQ ID No. 20 wherein the primer set is specific to RELB, SEQ ID No.21 and SEQ ID No. 22 wherein the primer set is specific to IRAK1, and SEQ ID No.23 and SEQ ID No. 24 wherein the primer set is specific to CASP9. An embodiment of the present invention provides the kit, wherein the amplified cDNA is measured for determining the upregulation of the one or more progressive and two or more TKI compliance biomarkers through high-throughput sequencing machines. Yet another important embodiment of the present invention provides a biomarker panel for determining compliance or non-compliance of tyrosine kinase inhibitors (TKI) treatment in a subject and/or for predicting or prognosing disease outcome for a CML patient for determining the activity, the stage, or the severity of CML in a subject, and/or for classifying a subject as a potential receiver or non-receiver of treatment for CML, wherein the biomarkers are both progressive biomarkers selected from but not limited to Shh, Gli-1, Smo, BCL-2, CD-34 and CCND-2, and/or any combination thereof and/or TKI compliance biomarkers are genes from the NFkB and apoptotic pathways and are selected from but not limited to RELA, FADD, BID, CASP9, IRAK1, FAS and BAD, or any combination thereof. In yet another embodiment, one or more gene or biomarker from the Shh pathway and target genes is used as a marker carrying out the methods of the present disclosure. In yet another embodiment, the compliance to treatment by a CML patient, particularly to TKI treatment and the CML disease progression is classified into the following categories: non- compliant, not-progressive; non-compliant, progressive; complaint, not-progressive; and compliant, progressive. In yet another embodiment, the results from the methods of the present disclosure and/or from the evaluation of the biomarkers from NF-kB pathway, Shh pathway, apoptotic pathways and voltage-gated ion channels expression provide important clinical indications that help in decision-making with respect to future course of treatment of the respective patient. In yet another embodiment, the method additionally comprises determining the progression of disease, compared to a previous recording of the disease level. In yet another embodiment, the genes, biomarkers or molecular markers employed in the methods of the present disclosure are identified using conventional molecular biology technique such as RT-PCR. All possible ways and means to carry out these techniques known to a person skilled in the art is envisaged by the method and assay of the present disclosure. Without limiting the scope of the present disclosure as described above in any way, the present disclosure has been further explained through the examples provided below. Example 1: Gene expression influenced by Imatinib In this study, the present disclosure analysed RNA-seq data using CML cell line K562 and Shh-K562 line, and CML- patient’s RNA-seq data available on European Genome-Phenome Archive (EGA). The molecular markers of therapy compliance in BCR-ABL leukaemia were identified. The Shh-pathway genes were also probed that may dispel chief information regarding disease progression. Shh-K562 in this study represents a model of Imatinib-resistant, progressive CML. The K562 and Shh-K562 cells were treated with Imatinib for 72 hours or not, to evaluate their relative gene-expression profiles (Figure 1). The density plot, volcano plot and heatmap represent the differentially expressed genes (Figure 1A-1C; up-regulated in red, down-regulated in Blue). The data here confirms that Imatinib can influence gene expression in cells. It was found that irrespective of the Shh-overexpression, expression of several genes is influenced by Imatinib treatment (Figure 1A-1C). Functional enrichment analysis performed using ToppGene Suite helped us to identify the different pathways that are up-regulated or down-regulated by Imatinib. It was found that different signalling pathways are influenced in presence or absence of Shh upon imatinib treatment (Figure 1D). Interestingly, a specific signalling pathway—namely Nuclear Factor kappa-light chain-enhancer of activated B-cells (NF-kB)-signalling is downregulated upon Imatinib treatment in cells with or without Shh-expression (Figure 1D, blue, bar-graphs). Since NF-kB-signalling down-regulation was consistently observed in presence and absence of Shh (Figure 1D), the pathway component was probed in more detail. NFkB is a well- recognized and studied pathway involved in the transcription of DNA, inflammatory response, innate immune system, and regulation of genes involved in cell survival and differentiation. Using KEGG pathway we identified the genes that belong to this pathway and compared their expression in our cell lines (Figure 2A). It was found find that several NF-kB genes are downregulated in presence of Imatinib (Figure 2A). To assess the in cells derived from CML patients, we analysed the RNA-seq data from Bradford et al (68 samples; Figure 2B). Down-regulation of these genes is observed in most of the patients in AP/BC-phase (expected to be on Imatinib) as opposed to the CP- patients at diagnosis (before Imatinib treatment; Figure 2C). It was found that even in CML-patient derived cells these genes are down-regulated in progressive patients, with or without drug binding site mutation. With similarity in down-regulation between the Imatinib-induced cell line and AP/BC patients, the attention was moved to the key players of the pathway, i.e., NF-kB subunits - RelA/p65, c-Rel, RelB, p50/p105/NFkB1 and p52/p100/NFkB2. These subunits were downregulated in the presence of Imatinib in the cell line. When CP (before Imatinib) and BC patients (on Imatinib) were compared, the BC patients showed Imatinib influence too, and the genes were all significantly downregulated except cRel (Figure 2C). Importantly, when we compared NF-kB pathway genes in matched samples collected at diagnosis (before Imatinib) and upon disease progression (on Imatinib), here again we find down-regulation in the expression of these genes (Figure 2D). These findings emphasizes that these can be used as potential markers of Imatinib-compliance, which if up-regulated would suggest noncompliance to Imatinib therapy. Further, other pathways that show Imatinib-mediated changes in gene expression profile in cell line and patient data were also looked into. Apoptosis and voltage-gated ion channel expression was also downregulated in presence of Imatinib. Here, select genes in apoptosis pathway are influenced by imatinib (Figure 3A). This narrowed down the search to intrinsic and extrinsic arm of apoptosis mentioned at KEGG by looking into FADD, BID, CASP9 and FAS, BAD respectively (Figure 3C). It is interesting to note that most of these genes that seemingly go down in the presence of Imatinib are pro-apoptotic in nature. This was observed in cell line models, CML-patients in AP/BC stages, and matched samples, when compared to samples collected at diagnosis from CP patients (Figure 3C). Likewise, several genes in voltage-gated ion channel subgroup are down-regulated in the presence of Imatinib (Figure 3B). We gave more weightage to some well-defined ion channels owing to their titular roles in the making of calcium- and sodium- gated channels respectively such as CACNB4, CACNB1, CACNA1D and SCN7A, SCN8A, SCN2B respectively. Canonical arm of Shh-pathway was put to scrutiny to assess the role of Shh signalling in CML patients and it showed up-regulation in majority of progressive patients, irrespective of the drug-binding mutation status (Figure 4A). This stresses on the fact that these genes can determine the progression status on a range of patients, regardless of the mutation status at BCR-ABL binding site. Major pathway components like, Gli1, Smo, BCL2, CD34, CCND2, etc. in patients showed significant upregulation in progressive patients (Figure 4B). Accordingly, it was proposed that expression of these genes from NF-kB, apoptosis and voltage gated ion channel classification can be used as markers of Imatinib compliance. Furthermore, the above results confirm the use of Shh-pathway components as predictable markers of disease progression. It was proposed that by using markers of non-compliance and progressive disease together it is possible to stratify the patients in timely manner. Our molecular markers of therapy compliance and progressive disease will be able to molecularly stratify CML patients into 4 categories to allow necessary therapeutic suggestion: Example 2: i.Materials and Methods The inventors have designed primer sets specific for the progressive and TKI compliant biomarkers: Table 1: List of primers designed for the generation of the cDNA library. Table 2: Characteristics and Target sequences for the primer sets Main stock: TE Buffer – Addition of 10mM Tris + 0.1mM EDTA and maintaining a pH- 8.0. From this main stock, the working stocks made in autoclaved with doubled distilled water. RNA isolation protocol: This protocol involves centrifuged 1.5-2 x 10 ⁶ cells at 1000 rpm for 5 mins. The supernatant discarded and the cells in the pellet were resuspended in 1X Phosphate Buffered Saline (PBS) as a wash step. Cells were harvested by centrifugation again at 1000 rpm for 5 mins and the supernatant is discarded. The pellet was resuspended in 1m Trizol (Ambion, life technologies, Thermo Fisher). Further, 0.2ml of chloroform was added to this mixture and mixed well. The mixture was incubated for 10 mins at room temperature, followed by centrifugation at 13,000 rpm for 15 mins at 4°C. The aqueous phase was carefully transferred to another centrifuge tube. To this aqueous phase, 0.5ml Isopropanol, 15µg/ml Glycoblue was added and mixed well and left standing for 15 mins. The mixture was centrifuged at 13,000 rpm for 30 mins at 4°C. The supernatant was decanted, and the pellet was washed with 70% Molecular grade Ethanol (EtOH, 1ml). This was further centrifuged at 13,000rpm for 5 mins, at 4°C. The supernatant was decanted, and the pellet was washed with 100% Molecular grade EtOH (1ml) followed by centrifuging at 13,000rpm for 5 mins, at 4°C. The supernatant was decanted and air drying the pellet till the smell EtOH is gone. The pellet was resuspended in 30-40µl of DEPC-H ₂ 0 and spun at 13,000rpm for 1° - 4°C to obtain the cellular RNA. The RNA concentration and purity (A260/A280 ratio) done using Nano-spectrophotometer (NanoDrop ^TM 1000 spectrophotometer) by using 1µl of the samples. The isolated and purified RNA were stored at 80°C. High-Capacity cDNA Reverse Transcription Kit with RNase Inhibitor A. To prepare the 2✕ RT master mix (per 20-µL reaction): 1. Allow the kit components to thaw on ice. 2. Referring to the table below for making the mix Table 3: Component Volume/Reaction (µL) Kit: B. To prepare the cDNA RT reactions: 1. Pipette 10 µL of 2✕ RT master mix into each well of a 96-well reaction plate or individual tube. 2. Pipette 10 µL of RNA sample into each well, pipetting up and down two times to mix. 3. Seal the plates or tubes. 4. Briefly centrifuge the plate or tubes to spin down the contents and to eliminate any air bubbles. 5. Place the plate or tubes on ice until you are ready to load the thermal cycler C. To perform reverse transcription: 1. Set the reaction volume to 20 µL. 2. Load the reactions into the thermal cycler. 3. Start the reverse transcription run. The following program conditions were used to perform the reverse transcription as embodied by the present invention. Table 5: Program the thermal cycler conditions: Components of PowerUp SYBR Green Master Mix - Applied Biosystems 1. Dual-Lock Taq DNA Polymerase 2. Heat-labile uracil-DNA glycosylase (UDG) 3. dUTP/dTTP 4. SYBR Green 5. ROX passive reference ii.TKI-compliance markers are downregulated by Imatinib in CML cell line. The differential gene expression profile was first observed in NGS based RNA-seq analysis of cell-line models, K562 and Shh-K562 as per the Examples 1. The inventors have identified genes that were significantly downregulated or not by performing RNA-seq analysis. The top 4 markers which were significantly downregulated in RNA-seq were chosen as the genes of interest—RELA, FAS, BID, CASP9; while 2 more markers were picked as negative controls as they were not significantly downregulated in RNA-seq analysis REL and IRAK1. These 6 TKI-compliance markers where then evaluated in RT-PCR based analysis using three different human cell-lines: 1. CML cell-line (K562 cells), with BCR-ABL translocation, myeloid lineage (experimental) 2. B-cell acute lymphoid leukemia (B-ALL) cells, with BCR-ABL translocation, lymphoid lineage (Control 1) 3. HEK-293T cells, Human cells without BCR-ABL translocation (Control 2). The inventors then tested the expression of the 6 genes-of-interest as TKI-compliance markers in all the three human cell-lines mentioned above. For this the cell-lines were treated with Imatinib in laboratory culture conditions, for 3 days or 6 days. The expression of genes was compared for each cell-line with their untreated control cells (Figure 5A and 5B). As observed in RNA-seq data, even in RT-PCR based approach, it was observed that there was significant suppression of RELA, FAS, BID and CASP9 expression. While the expression of IRAK1 or REL genes was not significantly affected by Imatinib, See Figure 5A. This RT-PCR based data is consistent with the RNA-seq data observed in example 1. To evaluate if the expression of genes can be upregulated again in absence of the drug by CML cell-line (K562), the imatinib was washed-off after 3 days of treatment and K562 cells were then cultured for 3 more days without Imatinib (See Figure 5A). It was found that when the imatinib was washed-off from the cells, it can indeed up-regulate the expression of the genes-of- interest. Thus, this data indicates that the identified genes-of-interest are sensitive to the presence or absence of drug. The relative expression these markers can thus be used to report the serum levels of TKI-drugs. It was observed that the cells in the lymphoid lineage with same causative translocation i.e., BCR-ABL+, SupB15 cells (grey bar, Figure 5B) or HEK-293T cells, without BCR-ABL translocation, do not show same behavior (black bar, Figure 5B). The inventors further picked RelA, FAS, BID from the above analysis as the markers for further analysis in CML patient’s peripheral blood. As expected from RNA-seq data, REL and IRAK1 are not significantly impacted by imatinib in RT-PCR. These two markers were hence dropped for further analysis using CML patient samples. Figure 5B shows that: RELA, FAS, CASP9 = Downregulated significantly in RT-PCR assay by CML cells, at 3 and 6day treatment. Also significantly downregulated in RNA-seq data (p-value: RELA = 0.00012; FAS = 0.000032; CASP9 = 0.000015). BID= Downregulated significantly in RT-PCR at 6days treatment (prolonged exposure to drug required) but not at 3days by CML cells and hence can represent prolong drug effect compared to RELA, FAS or CASP9. Also significantly downregulated in RNA-seq data (p-value: BID = 0.00000000024) REL = Not significantly downregulated in RT-PCR or RNA-seq data (p-value: REL = 0.5). IRAK1 = Not significantly downregulated in RT-PCR at 6days or RNA-seq data (p-value: REL = 0.019). Example 4: Method for evaluating relative expression of our proposed biomarkers in CML patients. The inventors further analyzed three TKI compliance markers, RELA, FAS, and BID in CML-patient’s peripheral blood. In this study, CASP9, which was present in example 3, was dropped as its behaviour was observed to be similar to RELA in RT-PCR based assay (Figure 5A). The inventors developed a method as per the embodiments of the present invention which can help in identifying reliably patients with differential regulation of TKI compliance markers and progressive markers. Here, the inventors have compared expression of proposed markers of TKI- compliance and Progressive disease in peripheral blood from 10 healthy donors. Shh-signalling pathway genes (Shh, Gli-1) and its target gene, Bcl2—an anti-apoptotic protein, known to impart resistance to TKI-drugs were used as progressive markers along with TKI-compliance markers. The study involved evaluation of the relative expression of 3-TKI compliance markers RELA, FAS, BID and 3- progressive markers Shh, Bcl2, Gli-1 in peripheral blood (PB) from 10 healthy donors by normalizing with their respective endogenous house-keeping gene, GAPDH. The median from the 10 healthy donors (X) and its standard deviation (sigma) were also derived. The raw score of the relative expression of the biomarkers genes for each CML patient independently (x) was identified again by normalizing their expression with the endogenous housekeeping gene, GAPDH. Finally, the normalized score of each gene-of-interest (x) was used to assign the z-scores to each gene, for each patient. This relative gene-expression levels allowed the inventors to identify patients with the relative fold change in the proposed markers. Table 6: Z-score based probability scores were used to assign the confidence in the inferences made and were calculated based on the formula: ^ = ^{×ି^} ఙ Wherein z = probability scores for up-regulation in gene expression x = gene expression in samples from CML patients X = median of gene expression in healthy subjects, σ = standard deviation of gene expression in healthy subjects Only probability of up-regulation in gene-expression is scored for making the calling. Probability of > 0.55 (i.e. > 55% chance of up-regulation in gene-expression) in any or all genes in Progressive biomarkers and/or at least two TKI-compliance biomarkers each is at least >55% is considered for making the respective callings. Based on the relative levels of the 6-markers, necessary action at the clinical level might be considered. Table 7: Conclusion: Accordingly, from the results obtained, it was inferred that upregulation of any of the 3 progressive biomarker or 2 or more of TKI-compliance biomarkers is necessary to make an assessment of progression of the disease and compliance to treatment. Based on these results, the medical practitioner can assess if patients are: 1. Compliant and non-progressive: are encouraged to continue medication. Such patients are likely to achieve deep molecular remission and can be considered for treatment-free remission after three or more years of treatment. 2. Non-compliant and non-progressive: Such patients can be warned, their irregular medication regime can be highlighted and such patients should be monitored more closely for progressive disease possibility. 3. Compliant but progressive: Such patients are considered molecularly distinct. This will mean, patients are taking the drug but are still likely to show progressive disease and so can considered for alternative therapeutic regime before it’s too late. 4. Non-compliant and Progressive: Such patients need alternative therapeutic regime before it’s too late. The comparison of the clinical trends of the 7-patients used for this analysis suggest that 6 of 7 patients molecular markers behaviour could predict the clinical trends. While the one patient (CML-6) is currently being monitored. It is important to evaluate the behaviour of these markers with necessary rigour using a larger CML- cohort based longitudinal follow-up study. Table 8: Although the disclosure and exemplification has been provided by way of illustrations and examples for the purpose of clarity and understanding, it is apparent to a person skilled in the art that various changes and modifications can be practiced without departing from the spirit or scope of the disclosure. Accordingly, the foregoing descriptions and examples should not be construed as limiting the scope of the present disclosure. The description of the embodiments of the present disclosure reveals the general nature of the embodiments that are readily suitable for modification and/or adaptation for various applications by applying the current knowledge. Such specific embodiments of the disclosure, without departing from the generic concept, and, therefore, such adaptations and modifications should and are intended to be comprehended and considered within the meaning and range of equivalents of the disclosed embodiments. As regards the embodiments characterized in this specification, it is intended that each embodiment be read independently as well as in combination with another embodiment. For example, in case of an embodiment 1 reciting 3 alternatives A, B and C, an embodiment 2 reciting 3 alternatives D, E and F and an embodiment 3 reciting 3 alternatives G, H and I, it is to be understood that the specification unambiguously discloses embodiments corresponding to combinations A, D, G; A, D, H; A, D, I; A, E, G; A, E, H; A, E, I; A, F, G; A, F, H; A, F, I; B, D, G; B, D, H; B, D, I; B, E, G; B, E, H; B, E, I; B, F, G; B, F, H; B, F, I; C, D, G; C, D, H; C, D, I; C, E, G; C, E, H; C, E, I; C, F, G; C, F, H; C, F, I, unless specifically mentioned otherwise. It is also to be understood that the phrases or terms employed herein are for the purpose of description and not intended to be of any limitation. Throughout the present disclosure, the word “comprise”, or variations such as “comprises” or “comprising” wherever used, are to be understood to imply the inclusion of a stated element, integer or step, or group of elements, integers or steps, but not the exclusion of any other element, integer or step, or group of elements, integers or steps. Where a numerical limit or range is stated herein, the endpoints are included. Also, values and sub-ranges within a numerical limit or range are specifically included as if explicitly written out. With respect to the use of any plural and/or singular terms in the present disclosure, those of skill in the art can translate from the plural to the singular and/or from the singular to the plural as is considered appropriate to the context and/or application. The various singular/plural permutations may be expressly set forth herein for the sake of clarity. Any discussion of documents, acts, materials, devices, articles and the like that has been included in this specification is solely for the purpose of providing a context for the present disclosure. It is not to be taken as an admission that any or all of these matters form a part of the prior art base or are common general knowledge in the field relevant to the present disclosure, as it existed anywhere before the priority date of this application. The contents of all references, patents, and published patent applications cited throughout this application are incorporated herein by reference for all purposes.