KRAS inhibitors such as Sotorasib and Adagrasib are reshaping the treatment landscape for G12C mutant cancers, yet durable responses remain limited by the emergence of drug tolerant persister (DTP) cells that survive initial therapy and drive relapse. Here, we identify a metabolic program centered on α ketoglutarate (α KG) that enables KRAS G12C–mutant pancreatic and lung cancer cells to withstand inhibitor pressure.