This strategy uncovered three candidate drugs for KMT2A-AML treatment improvement, including I-BET 151, a BET bromodomain inhibitor which inhibits BRD4, BRD2, and BRD3 as previously identified for KMT2A-r AML (Fu et al., 2015), sunitinib, a multitargeted kinase inhibitor (Papaetis and Syrigos, 2009), and quinacrine, an antimalarial drug that inhibits NFκB suppression of p53 (Oien et al., 2021), both being never explored in the KMT2A-r AML context. This evidence concerns the gene TP53 and acute myeloid leukemia.