In conclusion, our current study provided the evidence that TRIP expression was attenuated in RA-FLS compared with OA-FLS, and overexpression of TRIP significantly inhibited the activation of NF-κB signaling and decreased the production of proinflammatory cytokines and MMPs in TNFα-stimulated RA-FLS. This evidence concerns the gene NFKB1 and rheumatoid arthritis.