It is long been accepted that synovial inflammation, and the production of proinflammatory and destructive mediators from activated M1 macrophage, are of importance for the symptoms and progression of RA, while M2 macrophages mediate anti-inflammatory effects by producing anti-inflammatory cytokines such as IL-10 and TGF-β (4, 7). This evidence concerns the gene TGFB1 and inflammation.