Another known pathway where tumor cells maximize citrate synthesis, is through the excessive utilization of glutamine and glutamate to produce 2KG [32–36], an indirect precursor of citrate through the reductive carboxylation reaction catalyzed by IDH2 within the mitochondria and IDH1 within the cytosol (Fig. 1b) [31, 37–39]. The gene discussed is IDH1; the disease is neoplasm.