Indeed, TGF-β and IL-6-induced Th17 lymphocytes are less pathogenic and more exposure to IL-23 is needed for development of inflammatory Th17 lymphocytes.10,12 The relationship between IL-23/IL-17 axis and a number of autoimmune and inflammatory disorders including systemic lupus erythematosus,13 spondyloarthritis,14 psoriatic arthritis,15 Graves' disease,16 Crohn's disease,17 and EAE and MS18 has been reported. The gene discussed is IL37; the disease is Graves disease.