In the absence of this IL-1 regulatory mechanism, Tir8/Sigirr-deficient mice were more susceptible to experimental autoimmune encephalomyelitis (EAE) resulting from hyperactivation of Th17 cells upon immunization with myelin oligodendrocyte glycoprotein (MOG) peptide, which infiltrated the CNS in greater numbers and showed enhanced pathogenic functions compared to wild type Th17 cells (Gulen et al., 2010). The gene discussed is MOG; the disease is experimental autoimmune encephalomyelitis.