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. This evidence concerns the gene IL37 and spondyloarthropathy.