In joint inflammatory diseases (e.g., OA and RA), it is well documented that an excessive ECM proteolysis upon cellular stress or tissue injury generates ECM degradation products that act as damage-associated molecular pattern molecules or DAMPs (e.g., FN, tenascin C (TNC), proteoglycans) [33,34,35,36]. The gene discussed is TNC; the disease is rheumatoid arthritis.