Among the patients harboring TET2 mutations, MDS/MPN accounted for 58% (11 of 19), sAML evolved from MDS/MPN represented 32% (6 of 19), and MDS comprised 10% (2 of 19).44 However, TET2 mutations were infrequent in patients with solid tumors,50 despite somatic mutations in TET1(8 of 74), TET2(5 of 74), and TET3(4 of 74) were identified in colon cancer.51 Other molecular mechanisms underlying the dysregulation of TETs functions in both blood and solid cancers were diverse and complex such as metabolic alterations.52,53 These are discussed in the part of TETs function regulators. This evidence concerns the gene TET1 and myelodysplastic syndrome.