At present, the etiology of RA has not been fully elucidated, but what attracts attention is the immune processes that occur in the joint synovium and synovial fluid (3, 4), during which synovial macrophages release cytokines, such as tumor necrosis factor α (TNF-α), interleukin-1 (IL-1) and interleukin-6 (IL-6), which co-stimulate the activity of osteoclasts with inflammation and fibroblast-like synoviocytes (FLS), thus leading to the progress of bone erosion (5). This evidence concerns the gene TNF and rheumatoid arthritis.