Mutant IDHs catalyze the productionof the oncometabolite (2R)-hydroxyglutarate (R-2HG), which can accumulate to high levels (up to 30 mM).32,33 Elevated 2HG levels are proposed to inhibit 2OG oxygenases, includingthe TETs, in cells.34 The mutually exclusivenature of IDH and TET2 mutationsin AML is proposed to be due to functional redundancy31 in tumorigenesis and/or the synthetic lethality of TET1/3inhibition by R-2HG in TET2 mutantcells, which are reliant on TET1/3 for survival.35 TET inhibition is thus a potential strategy for treatmentof AML-bearing TET2 mutants. This evidence concerns the gene TET1 and acute myeloid leukemia.