Although Act1 is necessary for IL-17-mediated inflammatory responses, Act1−/− mice develop hyper Th17 responses (with increased IL-17 producing CD4+ T cells in lymph nodes and spleen) and spontaneous inflammatory/autoimmune diseases, including skin inflammation, SLE-like nephritis, and Sjögren’s-like disease3–6. This evidence concerns the gene TRAF3IP2 and nephritis.