Similarly, Bhatt et al. reported a shift in Bcl-2 interacting mediator of cell death (BIM) binding from Bcl-2 to Mcl-1 in venetoclax-resistant AML PDXs, emphasizing the need for concurrent inhibition of both Bcl-2 and Mcl-1 for optimal efficacy[115]. The gene discussed is MCL1; the disease is acute myeloid leukemia.