However, p53 is often lost or mutated in patients including therapy-related AML or AML with complex karyotype.27, 28 It has been demonstrated that MDM2 contributes to tumor initiation and progression even when p53 is no longer active.37 Our data confirm that MEG3 inhibits AML cell growth under genetic backgrounds of TP53 mutation, deletion or depletion, by decreasing MDM2 protein level. Here, MDM2 is linked to acute myeloid leukemia.