To date, a well characterized key inflammatory cascade in RA is overproduction and overexpression of TNF-α, enhancing interactions between T- and B-lymphocytes, synovial-like fibroblasts and macrophages, leading to synovial inflammation and joint destruction [3] and further promoting overexpression, release and activity of pro-inflammatory cytokines such TNF-α, vascular endothelial growth factor (VEGF), Interleukin-1β (IL-1β), IL-6, IL-8 and IFN-γ [4, 5]. This evidence concerns the gene TNF and rheumatoid arthritis.