As a result of abrogated Th1 responses, STAT4-deficient mice are resistant to the development of Th1-mediated autoimmune diseases, including EAE, RA, colitis, myocarditis, and diabetes, because they produce a smaller amount of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α). The gene discussed is STAT4; the disease is colitis.