KMT2A and leukemia: Another hallmark of MLL fusion oncogenes is their ability to recruit the H3K79 methyltransferase DOT1L to MLL target genes, which results in characteristically high levels of H3K79 methylation in MLL-rearranged leukemias and makes DOT1L an attractive therapeutic target (Daigle et al., 2011, Krivtsov et al., 2008).