Globally, Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are the most common potential target molecular subtypes in nonsmall cell lung cancer (NSCLC), with an incidence rate of 20%–25% in Western countries and approximately 10%–15% of cases in Asia.[1] KRAS functions as a critical cellular signaling switch, alternating between its inactive GDP‐bound form (GDP‐KRAS) and its active GTP‐bound form (GTP‐KRAS). The gene discussed is KRAS; the disease is non-small cell lung carcinoma.