At least in OCI-AML3 cells (representative of a recurrent AML genotype found in 10-15% of AML, NPM1, and DNMT3A mutant and TP53 wild type), we have shown an unexpected ability of BETi to directly potentiate activation of p53 by MDM2i, via relief of BRD4-mediated gene repression. Here, BRD4 is linked to acute myeloid leukemia.