Chronic myeloid leukaemia (CML) is probably one of the most comprehensively studied human malignancies. CML was the first human cancer that responds to molecular target therapy, Imatinib, a member of tyrosine kinase inhibitors (TKIs). Despite the excellent efficacy of TKIs, a subset of patients does not respond to TKIs, and are deemed to have resistance to the drug (Jabbour et al. 2008). Several mechanisms can play a role in the resistance to TKIs but the possible importance of drug-transporter proteins has been only recently appreciated with the demonstration that Imatinib is a substrate of P-glycoprotein (Pgp), the gene product of MDR1 gene. The generally accepted action of MDR1 is to reduce intracellular drug accumulation through Pgp-mediated efflux, thus hampering the achievement of effective drug levels at the target site (Ni L.N et al. 2011). Multi drug resistance gene (MDR1) ABCB1 product is an ATP-driven efflux pump contributing to the pharmacokinetics of drugs that are P-glycoprotein (P-gp) substrates (Eskazan et al. 2011). MDR1 inappropriate expression the P glycoprotein (Pgp) has been frequently implicated in resistance to different chemotherapeutic drugs as MDR1 single nucleotide polymorphisms (SNPs) are associated with drug clearance Imatinib has been reported to be a substrate of the P glycoprotein pump (Dulucq.et al. 2010). Identifying these SNPs may allow predicting drug disposition and responses to TKIs in CML patients.