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Discovery of the switch\u2010II pocket enabled the development of covalent KRAS G12C(OFF)\u2010state inhibitors, transforming a historically \u201cundruggable\u201d target into a therapeutic vulnerability. Drugging KRAS, however, proved to be a problem of chemistry, whereas sustaining its inhibition has proved to be a problem of biology. KRAS G12C\u2010mutant NSCLC is biologically heterogeneous, and the magnitude and durability of clinical benefit are shaped by co\u2010mutations, the tumor microenvironment, brain metastases status, pharmacologic differences between agents, and the dynamic evolution of resistance. Randomized trials have demonstrated that sotorasib and adagrasib improve progression\u2010free survival (PFS) and objective response rates (ORR) over docetaxel in previously treated disease, yet these gains have not translated consistently into a definitive overall survival (OS) advantage. This review synthesizes the epidemiology, molecular biology, diagnostic strategies, first\u2010 and later\u2010line treatment evidence, resistance mechanisms, and emerging KRAS\/RAS\u2010directed approaches. We distinguish randomized or guideline\u2010supported practice from early\u2010phase and translational signals, and propose an implementable framework that combines PD\u2010L1, tumor mutational burden, STK11\/KEAP1\/TP53 status, TTF\u20101 expression, brain metastases, and circulating tumor DNA (ctDNA) for risk stratification and mechanism\u2010guided management. At disease progression, oligoprogression should be distinguished from systemic progression, and tissue re\u2010biopsy together with plasma profiling should be considered when feasible. In China, several domestically developed KRAS G12C inhibitors have been approved, and reimbursement coverage is expanding; the cost of molecular testing, uneven institutional access, regional disparities and limited confirmatory and real\u2010world evidence nonetheless continue to constrain implementation. Future priorities include randomized first\u2010line comparisons, biomarker\u2010defined combination strategies, improved central nervous system activity and mechanism\u2010matched treatment after resistance.<\/jats:p>","DOI":"10.1002\/cai2.70082","type":"journal-article","created":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T05:59:35Z","timestamp":1792130375000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Molecular Mechanisms and Therapeutic Advances in KRAS G12C\u2010Mutant Non\u2010Small Cell Lung Cancer: Toward Mechanism\u2010Guided Longitudinal Management"],"prefix":"10.1002","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0009-0000-4134-2830","authenticated-orcid":false,"given":"Haiying","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Thoracic Medical Oncology Peking University Cancer Hospital Beijing 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