On the other hand, mutations of IDH1/2 shift redox homeostasis in cytosol and mitochondria, respectively, toward the more oxidated state due to the concomitant reduction of α-KG and the presence of high levels of 2-HG (2–600 μmol/L in AML patients’ serum) [45]. This evidence concerns the gene IDH1 and acute myeloid leukemia.