Th17 cells induced by TGF-β1/IL-6 (known as nonpathogenic Th17, non-pTh17) benefit the homeostasis of tissues in certain conditions while those induced by IL-1β/IL-6/IL-23 (known as pathogenic Th17, pTh17) promote the tissue inflammation and pathogenesis of RA (5–8). This evidence concerns the gene IL6 and rheumatoid arthritis.