We sought to validate this signature (and its constituent genes) across several independent conditions, drugs, and/or ex vivo functional and transcriptomic profiles of AML (Fig. 6), including a study by Lee and colleagues of drug sensitivity that profiled the BCL-2/BCL-XL inhibitor navitoclax31, the ex vivo study by Tavor and colleagues that profiled both venetoclax and navitoclax14, and a second FIMM dataset that profiled venetoclax and navitoclax in a stroma-derived conditioned medium (CM) that differed from the mononuclear cell medium (MCM) of the above FIMM dataset32. Here, BCL2L1 is linked to acute myeloid leukemia.