Interestingly, BCL2 was depleted in all AML cell lines except OCI-AML3, which carries a BAX pE41fs∗33 mutation (Figure 3E), suggesting BAX mutations as candidate mediators of resistance to BCL2 inhibitors, a promising therapeutic strategy in AML (Chan et al., 2015, Pan et al., 2014). Here, BAX is linked to acute myeloid leukemia.