In acute myeloid leukemia (AML), the p53 function is rarely disrupted by TP53 gene mutations, but more often by dysregulation of the nucleolar phosphoprotein nucleophosmin (NPM1) [1], the cellular p53 inhibitor MDM2 [2], the nuclear export protein XPO1/CRM1 [3], or the cytoplasmic retention protein CUL9/PARC [4]. Here, MDM2 is linked to acute myeloid leukemia.