KMT2A‐fusion oncogenes in acute leukemias either recruit DOT1L directly through their fusion partners, such as AF9, AF10, AF17, or ENL, or indirectly to their target genes, thereby fostering an active chromatin environment that counteracts transcriptional repression.70, 71, 72, 73, 74, 75, 76. This evidence concerns the gene KMT2A and acute leukemia.