Importantly, reactivation of p53 function represents a relevant strategy for AML therapy, since approximately 90% of de novo AML cases do not show a mutation in the p53 gene,28 but are rather characterized by an inactivation of the p53 pathway or deregulation of apoptosis-related genes.29 We demonstrated that reduction of CITED2 levels results in a decreased interaction between p53 and its inhibitor MDM2. Here, MDM2 is linked to acute myeloid leukemia.