Abstract
Chronic myeloid leukemia (CML) is characterized by the presence of the BCR-ABL1 oncoprotein, with constitutive activation of its tyrosine kinase activity and the neoplastic transformation of hematopoietic stem cells. The development of tyrosine kinase inhibitors (TKIs) specific for BCR-ABL1, such as imatinib mesylate, represented a breakthrough in the treatment of CML. However, therapeuti…