KMT2A fusion supports leukemogenesis by recruiting the superelongation complex (SEC), the histone H3K79 methyltransferase DOT1L and menin (MEN1), to induce the overexpression of AML TFs such as HOXA9, MEIS1, and MEF2C [9]. The gene discussed is KMT2A; the disease is acute myeloid leukemia.