Importantly, the tyrosine kinase (TK) activity is necessary for the transformation potential of BCR–ABL13, 4 Particularly, BCR–ABL1 TK activity induces a strong resistance to both intrinsic and extrinsic pathways of apoptosis,5 for instance, by inducing overexpression of BCL-XL6 and MCL-17 and downregulating TRAIL.8 Therefore, it is not surprising that the development of specific inhibitors directed to the TK catalytic site of BCR–ABL1, such as imatinib mesylate, revolutionized the treatment of CML patients.9 This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.