Given that most patients with hematologic neoplasms are TET2 haplodeficient and that TET1 and TET3 mutations are rare, it is likely that activating the residual TET2 or the other TET family members TET1 and TET3 may be a promising treatment strategy for TET2-deficient malignancies [131,132]. This evidence concerns the gene TET1 and hematopoietic and lymphoid system neoplasm.