PRDX2 and neoplasm: DNMT3AR882 mutations also enhanced abnormal stem cell gene expression, which promoted leukemia progression.147 Studies also found that DNMT3AR882 mutations reduced AML cell apoptosis by augmenting PRDX2,148 and induced CML by disturbing DNA methylation.149 In T-cell lymphomas, the DNMT3A mutation was found in both programmed cell death 1 (PD-1) + T cells and supportive cells, indicating its role in both tumor cells and microenvironment.150,151 Second, DNMT3A was found to be a haploinsufficient tumor suppressor in various hematologic malignancies.