On the other hand, GoF mutations or overexpression of EZH2 may often lead to a more aggressive disease phenotype, repressing tumor suppressor CDKN2A expression, which in turn is linked to HSC proliferation and self‐renewal [93], like in the case of MLL‐rearranged leukemias [94], suggesting that the PRC2 complex may act as an oncogene. This evidence concerns the gene KMT2A and leukemia.