For example, a recent preclinical study demonstrating that menin-MLL1 inhibition downregulated BCL2 and CDK6 and that CRISPR knockout or dTAG depletion of menin increased sensitivity to the BCL2 inhibitor venetoclax or the CDK6 inhibitor abemaciclib and further demonstrated synergistic effects of revumenib and related compounds in combination with venetoclax or abemaciclib in xenograft models derived from patients with MLLr or NPM1c AML (58). This evidence concerns the gene CDK6 and acute myeloid leukemia.