Somatic mutations in IDH1 or IDH2 result in the accumulation of an oncogenic metabolite, 2-hydroxyglutarate (2-HG), which can inhibit TET activity [10], and IDH1/2 mutations are strongly associated with the hypermethylator phenotype in glioma and AML [11–13]. The gene discussed is IDH1; the disease is acute myeloid leukemia.