Disruption of the MDM2–p53 interaction has been reported to serve as a promising tool in AML therapy30, 31 and various small molecules targeting p53 are currently implemented in the treatment of hematological malignancies to improve the efficiency of conventional cytotoxic drugs.32 One of the molecules used for targeting p53 is the MDM2–p53 inhibitor Nutlin3a and in this study we demonstrated that reduction of CITED2 expression sensitizes AML cells to Nutlin3a treatment. The gene discussed is CITED2; the disease is acute myeloid leukemia.