TRIP was reported to inhibit TNFα-induced NF-κB activation [27], and TNFα is involved in RA pathogenesis, so we evaluated the effects of TRIP overexpression on the production of proinflammatory cytokines and MMPs in TNFα-treated RA-FLS to investigate the potential role of TRIP in regulating inflammatory process in RA-FLS. The gene discussed is TNF; the disease is rheumatoid arthritis.