For example, CD109 has been found to have significant effects on rheumatoid arthritis; silencing CD109 or anti-CD109 treatment reduced the production of pro-inflammatory factors, cell migration, invasion, chemotactic attraction, and osteoclast differentiation, thereby decreasing the harmful inflammatory response of rheumatoid fibroblast-like synoviocytes (FLS) in vitro [58]. This evidence concerns the gene CD109 and rheumatoid arthritis.