Interestingly, it was also showed that TGF-β/Smad signaling contributes to BLM-induced fibrosis by promoting EMT, and recent studies demonstrated that TGF-β downregulated the IL-22 producing capacity of Th17 cells in both human [9, 10] and mouse systems [11] and inhibited the development of Th22 cells [12]. The gene discussed is TGFB1; the disease is Bloom syndrome.