Indeed, other studies have proposed a tumor suppressor role for EZH2, as loss-of-function mutations associated with decreased H3K27me3 levels were noted in patients with myelodysplastic syndromes and myeloproliferative neoplasms (MDS/MPN) [45, 46], and deletion of EZH2 was sufficient to induce MDS/MPN-like disease in mice [47]. This evidence concerns the gene EZH2 and neoplasm.