The interaction between MLLT10/AF10 and DOT1L was proposed to underlie the main molecular mechanism of leukemogenesis by the MLL-MLLT10/AF10 and CALM-MLLT10/AF10 fusions [30],[33]; mis-targeting of DOT1L and the resulting activating H3K79 methylation causes aberrant activation of target genes, such as Hoxa5, leading to leukemia. The gene discussed is KMT2A; the disease is leukemia.