Since treatment with SNDX-50469 was associated with inhibition of protein levels of BCL2 in MOLM13 and OCI-AML3 cells, we investigated whether this sets up these cells to be more susceptible to the inhibitory activity of co-treatment with venetoclax on the residual BCL2 levels, as well as increasing anti-AML efficacy of the combination of SNDX-50469 with venetoclax in AML cells expressing MLL-FP or NPM1c. This evidence concerns the gene RUNX2 and acute myeloid leukemia.