Studies in animal models of MS (i.e., experimental autoimmune encephalomyelitis, EAE), evidenced that osteopontin administration induces disease reactivation [21] and osteopontin-deficient mice showed a milder disease course with decreased inflammatory infiltration, reduced expression of tumor necrosis factor and interferon gamma, and increased production of the anti-inflammatory IL-10 [22,23]. The gene discussed is SPP1; the disease is experimental autoimmune encephalomyelitis.