Studies have shown that MET gene amplification activates the ErbB3/PI3K/AKT signaling pathway, triggering resistance to EGFR kinase inhibitors. Because of the association between c-MET gene amplification and poor prognosis in NSCLC and resistance to epidermal growth factor receptor (EGFR) inhibitors such as erlotinib, c-MET receptor tyrosine kinase has become an interesting anticancer target in NSCLC treatment. Small molecule inhibitors targeting MET are currently in phase II/III clinical studies. ARQ197 is a novel selective c-MET inhibitor. 2011 study published in JCO showed that the median progression-free survival of patients in the erlotinib + ARQ197 group was 16.1 weeks compared to 9.7 weeks in the erlotinib + placebo group (HR=0.81, p=0.24, corrected HR=0.68, p<0.05). Patients with non-squamous cancer, wild-type EGFR gene and positive K-ras gene mutation had significantly better PFS than other patients, and there was no significant difference in adverse effects between the two groups. Follow-up 34 patients who failed erlotinib treatment were crossed over to the erlotinib combined with ARQ197 treatment group, and 2 PRs and 9 SDs occurred in 23 patients with evaluable efficacy. 2 of the PRs had c-Met amplification, suggesting that c-Met small molecule inhibitors are a reasonable choice for patients who failed TKIs. MetMAb is a monovalent monoclonal antibody that specifically binds to the Met receptor, and the results of the OAM4558g study presented at the 2011 ASCO annual meeting showed that MetMAb in combination with trospium significantly improved PFS and OS in patients with c-Met expression-positive NSCLC, reducing the risk of death in such patients by nearly 3-fold. met FISH+/IHC+ and Met FISH-/IHC+ patients also benefited, suggesting that IHC results are a sensitive predictor of MetMAb efficacy. Corresponding phase III clinical studies are currently underway.