This TKI directly inhibits the BCR-ABL1 fusion oncogene by blocking its ATP-binding pocket and repressing its signaling [66, 67], thereby upregulating BIM at transcriptional and posttranslational levels to induce CML cell death [8, 12, 68]. This evidence concerns the gene BCL2L11 and chronic myelogenous leukemia, BCR-ABL1 positive.