KMT2A and leukemia: Recently, the MLL gene can recombine with more than 60 partners to acquire abnormal gain-of-function effects on aberrant epigenetic modification and proto-oncogene activation, as a result triggering dysregulated increased expression of the clustered homeobox A (HOXA) genes, which results in limitless self-renewal capacity necessary for leukemia initiation and propagation [3].