Recent studies show that IL-25-deficient (Il25-/-) mice are highly susceptible to experimental autoimmune encephalomyelitis (EAE), a mouse model for human MS, while neutralization of IL-17A prevents EAE in IL-25-deficient mice, indicating a role of IL-25 in attenuating inflammation by inhibiting Th17 function (48). The gene discussed is IL25; the disease is experimental autoimmune encephalomyelitis.