Reflecting the function as T cell activator, the development of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), is improved in Sema4A-deficient mice partly due to impaired Th1 and Th17 differentiation [6, 10]. This evidence concerns the gene MOG and myeloid sarcoma.