Since SIPA1 can interact with MET, and SIPA1 can regulate the MET receptor protein, and the inhibition of SIPA1 has similar effects on the TJs of lung cancer cells as the MET inhibitor Crizotinib, it is possible that SIPA1 may be a potential therapeutic target in NSCLC and a potential substitute target for MET targeted therapy resistance in NSCLC. The gene discussed is MET; the disease is lung cancer.