Although HDACs mutations occur also exceptionally rarely in children with AML, myeloid oncoproteins and leukemia-associated fusions can recruit HDACs abnormally, such as EVI1, RUNX1::RUNX1T1 (previously AML1::ETO), so as to block differentiation and maintain the leukemic phenotype of AML (38). The gene discussed is RUNX1; the disease is acute myeloid leukemia.