Glutamine catabolism, which starts with the hydrolysis of glutamine to glutamate catalyzed by the glutaminase family of enzymes, becomes highly upregulated in cancer cells to compensate for the uncoupling of the glycolytic pathway from the TCA cycle due to the Warburg effect, thus providing the biosynthetic precursors necessary for their enhanced proliferation and survival7–10. The gene discussed is GLS; the disease is cancer.