KIT mutations constitute driver events in SM pathogenesis and are mechanistically implicated in AML1-ETO+ AML, explaining their frequent co-occurrence.While the KIT D816V mutation predominates in adult SM (>80% prevalence), pediatric SM exhibits markedly lower D816V incidence coupled with higher frequencies of non-canonical KIT variants (1). This evidence concerns the gene RUNX1 and acute myeloid leukemia.