As a third-generation tyrosine kinase inhibitor, ponatinib eliminates BCR-ABL wild-type and mutant (BCR-ABLT315I) CML cells more effectively than first- and second-generation BCR-ABL tyrosine kinase protein inhibitors, thus reducing the evolution of resistance that may result from drug exclusion [227]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.