Patients with OA also exhibited high concentrations of lectin complement pathway components, including mannose bindin lectin (MBL), H-ficolin, M-ficolin, mannan-binding lectin serine protease- 2 (MASP-2), and MASP-3, which were higher in the plasma than the SF [54], and while the levels were significantly lower than patients with RA, this data suggests a possible role of the lectin pathway in promoting chronic disease in knee OA. This evidence concerns the gene FCN1 and rheumatoid arthritis.