In the synovium of RA patients, nuclear factor kappa B (NF-κB) promotes the proliferation of synovial fibroblasts and stimulates osteoclast formation, which in turn increases the expression of inflammatory factors such as IL-1α, IL-1β, IL-6, IL-17, and TNF-α, leading to bone destruction [7,8,9,10]. This evidence concerns the gene TNF and rheumatoid arthritis.