Upregulation of SEMA4D following spinal cord injury [37, 38] has been reported, and interactions between SEMA4D and PLXN-B1 and -B2 receptors have been implicated in neuroinflammation and pathogenesis of experimental autoimmune encephalomyelitis [32, 39]. The gene discussed is SEMA4D; the disease is experimental autoimmune encephalomyelitis.