In fact these and other studies show that the absence of IFN-γ exacerbated the disease severity in many IL-17 mediated autoimmune diseases including RA [3, 8, 9] while other recent reports still suggest a role for IFN-γ due to the presence of auto antigen specific Th1 cells in RA [12]. The gene discussed is IL17A; the disease is rheumatoid arthritis.