Anti-SEMA4D monoclonal antibody therapy has been shown to inhibit activation of glial cells and ameliorate neurological disorders in several in vivo experimental models, including a transient middle cerebral artery occlusion mouse model of stroke [19], lysolecithin-induced rat spinal cord lesions, experimental autoimmune encephalomyelitis (EAE) [13], and the YAC128 transgenic model of Huntington’s disease [17]. The gene discussed is SEMA4D; the disease is nervous system disorder.