Experimental evidence suggests that NF-κB activation plays a pivotal role both at the stage of initiation and the stage of perpetuation of chronic inflammation in RA, including development of T helper 1 responses, activation, abnormal apoptosis and proliferation of RA fibroblast-like synovial cells, and differentiation and activation of bone resorbing activity of osteoclasts. This evidence concerns the gene NFKB1 and rheumatoid arthritis.