Notably, one patient with acquired <i>MET</i> amplification achieved a renewed partial response to the combination of sotorasib and tepotinib after progression on sotorasib monotherapy.<h4>Conclusion</h4>This study provides real-world evidence that <i>MET</i> amplification is an acquired and potentially targetable resistance mechanism to KRAS G12C inhibition in NSCLC. The gene discussed is KRAS; the disease is non-small cell lung carcinoma.