This beneficial antigouty arthritis effect might be mediated, at least in part, by inhibiting TNF-α, IL-1β, IL-8, and NF-κB p65 protein expression in synovial fluid and synovial tissue, and the suppression of NF-κB might be responsible for the decrease of the levels of IL-6, IL-8, and TNF-α in synovial tissue. Here, NFKB1 is linked to arthritic joint disease.