For example, tumor necrosis factor (TNF), interferons (IFNs), interleukin (IL) -1β, IL-2, IL-4, IL-6, IL-8, IL-17, IL-18, IL-21, IL-22, IL-23 and granulocyte macrophage-colony stimulating factor (GM-CSF) have been suggested to play a central role in RA pathogenesis (6–8). This evidence concerns the gene IL17A and rheumatoid arthritis.