In MLL-rearranged leukaemia, aberrant recruitment of DOT1L by fusions also requires the action of the ubiquitination machinery for DOT1L to access chromatin, where it operates as an essential component of MLL fusion target gene activation through the deposition of its gene-activating H3K79 methylation mark [[170], [171], [172]]. This evidence concerns the gene KMT2A and leukemia.