Current evidence suggests that IL-22 plays a pathogenic role in RA, in that IL-22 levels are increased in serum and synovial fluid of patients with RA compared to controls, IL-22 induced RANKL and the increased levels of IL-22 correlated with disease activity and bone erosions [14], [15], [16], [17], [18]. The gene discussed is TNFSF11; the disease is rheumatoid arthritis.