In the current study, we have analyzed and compared the genetic, phenotypic, and transcriptomic features of AML driven by a combination of FLT3ITD TET2, FLT3ITDDNMT3A, or FLT3ITD TET2 DNMT3A, utilizing AML models, patient cells, and transcriptomic data derived from both mice and humans. The gene discussed is TET2; the disease is acute myeloid leukemia.