Currently, several mechanisms for the imatinib resistance observed in patients with CML have been studied such as mutations on the BCR-ABL kinase domain, increased BCR-ABL expression, and overexpression of drug-efflux proteins (ABCB1 and ABCG2) [32]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.