We hypothesized that it may be related to the self-production of proinflammatory cytokines by RA-FLS, even without IL-1β administration; the low dose of cytokines could also promote the expression of USP5 and facilitate the interaction between TRAF6 and USP5, which also indicated that USP5 is crucial for the inflammatory processes of RA-FLS. Here, IL1B is linked to rheumatoid arthritis.