The outcome of this cooperation has been functionally evaluated in TET2 KO mice harboring one of these mutations, such as Flt3ITD [130], Asxl1 [131], JAK2V617F [132], Ezh2 [133], Nras [134], KITD816V [135], RhoAG17V [136], DNMT3AR882H [137], SRSF2P95H [138], AML-ETO [139], etc. Overall, when combined with a TET2 LOF, these mutations substantially accelerated the development of various types of hematologic neoplasms with significantly shortened latencies; major phenotypes of the mice are summarized in [93]. The gene discussed is TET2; the disease is acute myeloid leukemia.