The remarkable correlation of H3K79me2 and MLL targets has been referred to as a special epigenetic lesion in MLL leukaemia, implying the essentiality of H3K79 methylation for MLL-driven transcription.35 Inactivation of DOT1L profoundly suppressed the expression of MLL translocation-associated genes (for example, HOXAs and MEIS1) and leukaemia development36, 37, 38, 39, 40 (Figure 1a). Here, KMT2A is linked to leukemia.