The profound hypermethylation status of Tet2 and Tet3 double-knockout HSPCs and full-blown AML development in Mx1CreTet2fx/fxTet3fx/fx mice suggest the compensatory effects of Tet2 and Tet3 in the differentiation of early myeloid progenitors [20]. The gene discussed is TET2; the disease is acute myeloid leukemia.