The activators bind all antiapoptotic BCL-2 family members, whereas the sensitizers NOXA and HRK are more selective in binding MCL-1 and BCL-XL, respectively.11 BCR-ABL modulates the expression levels and/or the phosphorylation status of several BCL-2 family members, thus exerting important regulatory effects on apoptosis.12, 13, 14, 15 Furthermore, recent reports suggest important roles for several antiapoptotic BCL-2 family members in CML disease progression.16, 17, 18, 19, 20 Elevated levels of these proteins in several cancers make them promising targets for drug therapy. This evidence concerns the gene BCL2L1 and chronic myelogenous leukemia, BCR-ABL1 positive.