In MLLr and NPM1 mutant leukemias, however, Hox gene expression is aberrantly activated either by the MLL fusion proteins or by aberrant wild-type MLL activity mediated by NPM1 mutants, inhibiting differentiation and resulting in increased cell proliferation and survival that drives leukemogenesis [125,137,138,139,140,141,142,143,144,145]. Here, KMT2A is linked to leukemia.