Remarkably, TET proteins (TET1–3), particularly TET2, have been recognized as tumor suppressors in the hematopoietic lineage, with inactivating mutations occurring in a significant proportion of patients with myelodysplasia (MDS), acute myeloid leukemia (AML), and clonal hematopoiesis of indeterminate potential (CHIP), a premalignant condition found in approximately 10% of elderly individuals that increases their AML risk [172,173,174]. This evidence concerns the gene TET1 and acute myeloid leukemia.