In macrophages, the activation of NF-κB in response to Toll-like receptor (TLR) ligands, such as LPS, results in the transactivation of a number of cytokines, chemokines, and other pro-inflammatory mediators (15, 16), and it was reported that TLR4 was activated in RA (16). Here, NFKB1 is linked to rheumatoid arthritis.