The reliance on glutamine metabolism presented by cancer cells can be altered in the GBM-IDH mutant, since IDH1/2 mutated enzymes use α-ketoglutarate as a substrate to produce the oncometabolite 2-hydroxyglutarate (D2-HG), therefore a higher commitment of glutamine-derived glutamate is needed to produce α-ketoglutarate that will not be used in the TCA cycle, as will be depicted later on in this review. The gene discussed is IDH1; the disease is cancer.