Recently, targeted therapy and immunotherapy have significantly improved the prognosis of patients with non-small cell lung cancer. In addition to epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), c-MET or MET is another important target for non-small cell lung cancer. MET plays an important role in the occurrence of lung cancer, affecting the proliferation, invasion, and angiogenesis of cancer cells. In non-small cell lung cancer, the mechanism of abnormal activation of the MET signaling pathway includes overexpression of MET or hepatocyte growth factor (HGF) protein, MET gene amplification, MET gene mutation, MET rearrangement, abnormal downstream signaling, and abnormal regulatory components. Drugs targeting MET include selective tyrosine kinase inhibitors (TKIs), non-selective TKIs, and antibodies against MET or its ligand HGF. Besides, the drug resistance mechanism to new drugs is also worthy of further study.