These findings support additional testable hypotheses that combinations with other MDM2 inhibitors or inhibitors of MYC signaling, such as a bromodomain and extra-terminal motif inhibitor (BETi), might synergize with selinexor in AML and other tumor types with functional p53 through alleviation of suppression of p53 activity. The gene discussed is MYC; the disease is acute myeloid leukemia.