Ablation of H3K79 methylation through knockout or pharmacological targeting of DOT1L abrogates the MLL-fusion target gene expression profile, selectively induces apoptosis and differentiation of leukemia cells in culture and dramatically extends the survival of mice in xenograft experiments (Bernt et al., 2011; Daigle et al., 2013). This evidence concerns the gene KMT2A and leukemia.