CML treatment involves three critical elements: the discovery of the underlying molecular genetic defect (BCR-ABL fusion gene); development of therapies to attenuate the enhanced kinase activity caused by this defect (imatinib and second/third generation BCR-ABL kinase inhibitors); and the use of imatinib in newly diagnosed diseases that have not undergone genomic evolution. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.