The development of resistance to Imatinib in CML is a multifactorial process, including point mutations in the structural domain of BCR–ABL kinase, amplification of the BCR–ABL gene, and the presence of leukemic stem cells that can produce Imatinib-insensitive active mutants [36,37]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.