Similarly, Muto et al supported that deletion of EZH2 was sufficient to induce MDS/Myeloproliferative neoplasm (MDS/MPN) in transgenic mice [31], whereas Soverini et al reported loss-of-function mutations of EZH2 gene in chronic myeloid leukemia [32] further supporting the hypothesis that EZH2 inactivation may be implicated in chronic myeloid dysplasia and hyperplasia. This evidence concerns the gene EZH2 and myeloproliferative neoplasm.