In the nucleus, activated NF-κB binds to the promoter regions of target genes, facilitating the transcription of many inflammatory cytokines, including TNF-α, interleukin 1β (IL-1β), and IL-6 increased expression of these cytokines, leading to amplification of the inflammatory response, as well as the stimulation of synoviocytes proliferation and production of matrix metalloproteinases, thus facilitating inflammation and joint damage in RA (88). This evidence concerns the gene IL1B and rheumatoid arthritis.