Many of these molecules have been found increased in RA tissues; administration of danger signals, such as fibronectin EDA or tenascin-C, induces joint inflammation in vivo, while mice deficient in tenascin-C show a rapid resolution of inflammation (Goh and Midwood, 2011), indicating an important role for ECM molecules as initiator/amplifiers of the autoimmune process in RA. This evidence concerns the gene FN1 and rheumatoid arthritis.