The importance of this difference has been made clear by several autoimmune disease models such as collagen-induced arthritis (CIA) and experimental autoimmune encephalomyelitis (EAE), where ablation of IFN-gamma resulted in exacerbated disease due to increase in production of mature IL-1β and IL-17, as well as enhanced T cell proliferative responses [65]. The gene discussed is IL1B; the disease is autoimmune disease.