However, ~30–40% of patients fail to respond optimally to IM treatment.[1] The majority of research on imatinib resistance in CML has been focused on identifying methods to overcome resistance driven by BCR-ABL kinase domain mutations through the use of second and third generation tyrosine kinase inhibitors (TKIs), including dasatinib, nilotinib, ponatinib, and others. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.