In CML, BCR-ABL upregulates Bcl-2 [64] and Bcl-XL [65] through activation of STAT5, and inhibits release of cytochrome C [66] and prevents caspase activation even after cyto C release [67], hence confering resistance to apoptosis to CML cells. This evidence concerns the gene BCL2L1 and chronic myelogenous leukemia, BCR-ABL1 positive.