While p53 haploinsufficiency or loss strongly promoted the leukemogenesis of FLT3-ITD (shortened survival and high incidence of AML, Fig. 1), Nabinger et al reported that p53R248W mutation did not cooperate with FLT3-ITD to induce AML and to reduce the survival of mice [6]. The gene discussed is FLT3; the disease is acute myeloid leukemia.