Overexpression of KIT-AL mutant has been shown to cooperate with RUNX1-RUNX1T1 or CBFB-MYH11 to induce AML in mice.21, 22 However, KIT mutations are known to be unstable during disease evolution, with nearly 50% of cases losing or changing their mutations at relapse.10 The mechanistic link between KIT-AL mutations and inferior prognosis in CBF-AML would have to be further elucidated. The gene discussed is RUNX1; the disease is acute myeloid leukemia.