TET2 and myeloid neoplasm: In the recent years, several lines of experimental evidence have demonstrated that TET2 mutations can be detected in a significant number (12–34%) of myeloid malignancies and lead to DNA hypomethylation1 and subsequently to an open chromatin reading frame (increased chromatin accessibility associated with TET2 mutations), which is known to be a critical driver for malignant HSC self-renewal and carcinogenesis.2