Among its three members, TET2 acts as a tumor suppressor and is mutated in a wide range of hematological malignancies.41, 42 Loss of function analyses revealed that TET2 and TET3 have redundant roles in hematopoietic system and can compensate for one another.42 A miR-15b–TET3–cyclin D1 axis is important for neocortical development, where miR-15b reduces TET3 expression and 5hmC levels and regulates neural progenitor proliferation through epigenetic control of cyclin D1 expression.43 Whether miR-150–TET3 functions in epigenetic regulation in leukemia is under investigation. Here, TET2 is linked to neoplasm.