Tumor suppressor genes slow down cell division, to allow for the repair of DNA mistakes or induction of apoptosis in case of severe cell damage. Mutations in the tumor suppressor gene TP53 rarely occur in de novo AML but are common with therapy-related AML or AML with myelodysplastic-related changes. They are commonly associated with complex cytogenetics, older age, chemoresistance, and poor survival. Treating patients with TP53­-mutations is a high unmet need.