NF-κB p65 can then move to the nucleus and bind to target genes, which can enhance the expression level of many inflammatory mediators (such as TNF-α, IL-1β, COX2, etc.)expressed in the synovium of rheumatoid arthritis.[31] Furthermore, it has been suggested that NF-κB p65 regulates cell apoptosis and inhibits protein expression, having an antagonistic effect on the apoptosis of FLS-RA cells. Here, IL1B is linked to rheumatoid arthritis.