were described in many inflammatory autoimmune diseases such as Crohn's disease [6], rheumatoid arthritis [21], and multiple sclerosis [22]. In vitro experiments suggested that in the presence of low amounts, or in total absence of TGF-β, IL-12 and IL-23 cytokines induced the conversion of Th17 cells toward a Th1 phenotype whereas sufficient TGF-β quantities maintained a Th17 phenotype [6, 21, 23]. The gene discussed is TGFB1; the disease is rheumatoid arthritis.