Kerr and colleagues showed that KRAS G12D copy gain, which is a common step during tumor progression, not only induces a glycolytic switch in lung cancer models, but also enhances glutathione (GSH) biosynthesis, translating into lower ROS levels and increased resistance to oxidative stress; treating KRAS-mutant NSCLC cell lines with the glucose analogue 2-deoxy-D-glucose and with BSO (an inhibitor of the synthesis of GSH) resulted in a dramatic apoptosis, confirming their dependency on glucose and GSH (115). The gene discussed is KRAS; the disease is lung cancer.