Rheumatoid arthritis (RA) is an inflammatory autoimmune disease, in which the proinflammatory transcription factors nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and activator protein-1 (AP-1) are activated by inflammatory cytokines, which in turn upregulate the expression of these cytokines, thereby assembling a positive feedback loop perpetuating inflammation [1,2]. This evidence concerns the gene NFKB1 and rheumatoid arthritis.