Targeting c-MET activity with small molecule inhibitors adversely disrupts tumor proliferation, neovascularization, and distal metastasis across different cancer types, including gastric, breast, hepatic, pancreatic, and lung carcinomas, suggesting that HGF/c-MET axis is a crucial survival expedient for tumor cells in hypoxic TME 53. This evidence concerns the gene HGF and lung carcinoma.