Lung cancer has the highest incidence and mortality rate among malignant tumors worldwide. Of these, non-small cell lung cancer (NSCLC) accounts for 80% to 85%. The vast majority of NSCLC is already advanced at the time of initial diagnosis, and even in early stage patients, most will develop recurrence or metastasis during the course of the disease and become advanced NSCLC, for which chemotherapy is the primary treatment in this patient population. However, the platinum-containing two-drug combination chemotherapy regimen, which is the standard first-line treatment, has entered the plateau stage, with progression-free survival (PFS) of 4-6 months and overall survival (OS) of only 8-10 months, making it difficult to obtain a more significant improvement. In recent years, the clinical application of molecularly targeted drugs has given people hope and light to cross this plateau. With appropriate molecular targeted therapy, the overall survival of patients with advanced NSCLC has exceeded 12 months, and some patients even get several years of progression-free survival. However, unlike traditional chemotherapeutic agents, molecularly targeted drugs have more specific target selectivity and significant individual differences in patient outcomes, making the selection of patient populations for molecularly targeted therapy critical. Some of these biomarkers have been successfully applied in the clinic to screen for the most favorable population for a particular molecularly targeted therapy. It is these biomarkers that make it possible to individualize molecularly targeted therapy for NSCLC. No. Test item Clinical significance Relevant drugs 1. EGFR gene exon 19/21 mutation Studies have shown that patients with EGFR tyrosine kinase gene coding region exon 19 or 21 mutation in lung cancer tissues can be treated with EGFR-TKI with an efficiency of more than 80%; while the efficiency of non-mutated patients is less than 10%. Gefitinib (ERSA) Erlotinib (Troche) 2. EGFR gene exon 20 T790M mutation Studies have shown that EGFR exon 20 T790M mutation is the main cause of secondary resistance to targeted drugs in patients. 50% of lung cancer patients have EGFR exon 20 T790M mutation rate. 3. KRAS codon 12/13 mutations NCCN states that the mutation rate of KRAS in lung cancer is 15-30%. The mutations that cause KRAS to be activated are mainly located in codon 12/13 of the exons, and the mutations will likely cause resistance to targeted therapy in lung cancer. Gefitinib (ERSA) Erlotinib (Troche) Cetuximab (Ebitux) Panitumumab (Vikotib) 4. Mutations in the BRAF gene V600E Mutations in the KRAS gene downstream of the EGFR signaling pathway cause patients to become resistant to cetuximab and panitumumab therapy, but some patients without KRAS mutations also become resistant to such targeted agents. Further studies suggest that the development of resistance is due to the V600E mutation in the BRAF gene. This mutation may also have application in treatment-guided lung cancer targeted therapy selection. Gefitinib (Erisa) Erlotinib (Troche) Cetuximab (Eptifib) Panitumumab (Vikotib)