BCR::ABL1 confers a survival advantage to CML cells in part through changes to the BCL-2 proteins [16], particularly through upregulation of BCL-2 [17, 18], MCL-1 [19], and BCL-xL [20, 21], and downregulation of BIM [22–24]. This evidence concerns the gene MCL1 and chronic myelogenous leukemia, BCR-ABL1 positive.