And Cyr61 secreted by FLS subsequently stimulated the production of various proinflammatory mediators (IL-17, IL-6, IL-8, and IL-1β) through Akt/NF-κb and MAPK signaling pathways and thereby participated in the pathologic mechanism in RA [7–9, 17]. The gene discussed is CCN1; the disease is rheumatoid arthritis.