Induction of Th17 cells by TGF-β1 and IL-6 in vitro is not sufficient to cause autoimmune tissue injury in experimental autoimmune encephalomyelitis (EAE), but when induced by IL-1β, IL-6, and IL-23 or TGF-β3, Th17 cells trigger EAE, consistent with the critical roles of IL-23 signaling in the terminal differentiation of Th17 cells17, 20–23. This evidence concerns the gene IL6 and experimental autoimmune encephalomyelitis.