In fact, because of the strict association at diagnosis, and stability upon relapse, of essentially all Flt3mutant AML’s with accompanying epigenetic mutations within IDH2/TET2/WT1 pathway or, additionally, with DNMT3A or ASXL1 mutations, this regimen, or a very similar one, may have broad applicability for sensitivity “priming” [43,44]. The gene discussed is TET2; the disease is acute myeloid leukemia.