The tyrosine kinase inhibitor imatinib has been developed with remarkable effects in CML treatment; however, point mutations in the tyrosine kinase domain of BCR-ABL and/or high expression of BCR-ABL mRNA usually induce resistance to tyrosine kinase inhibitors [5,6,7,8]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.