Deletion of Tet2 in mice leads to sporadic development of MDS/CMML-like disease [13–16] and co-expression of mutated Tet2 with additional oncogenic mutations, including Asxl1, Ezh2, Jak2, c-Kit, Flt3, Bcor, Sf3b1, and AML1::ETO, promotes disease in mice [12, 17, 18]. The gene discussed is TET2; the disease is myelodysplastic syndrome.