TP53 and acute myeloid leukemia: Reconstitution of p53 tumor-suppressor activity, through treatment with the MDM2 antagonist idasanutlin, and induction of mitochondrial apoptosis, through specific Bcl-2 inhibition with the BH3 mimetic venetoclax, led to anti-tumor effects in both in vitro and in vivo human xenograft models of AML.