r-hirudin and DTIP could bind to thrombin specifically and block thrombin binding to PAR-1, thereby inhibiting NF-κB activation and reducing the expression of N-cadherin and snail, while increasing the expression of E-cadherin in NSCLC cells, and this mechanism is very beneficial for suppressing VM formation. The gene discussed is NFKB1; the disease is non-small cell lung carcinoma.