We found that exposure of BCP-ALL cell lines to venetoclax at low nanomolar concentrations resulted in enhanced mitochondrial cytochrome c release by HRK and MS1 (median delta priming 27% for HRK and 75% for MS1), demonstrating a switch from BCL-2 dependence to combined dependence on BCL-XL and MCL-1 in the presence of venetoclax (Fig. 3B). Here, BCL2L1 is linked to acute lymphoblastic leukemia.