Interestingly, clinical and preclinical evidence suggests that this spectrum of oncogenic KRAS point mutations (capable of driving tumorigenesis) is often exploited to reactivate RAS signaling and drive resistance following treatment with KRAS mutant-selective therapies, e.g., in patients with KRASG12C NSCLC tumors treated with sotorasib, adagrasib, or divarasib (22, 23, 37). The gene discussed is KRAS; the disease is non-small cell lung carcinoma.