On the other hand, TRAIL blockade with the administration of soluble rTRAIL receptor, during the effector phase of MOG-induced experimental autoimmune encephalomyelitis (EAE), enhances the formation of inflammatory lesions and the extent of demyelination in the CNS, and exacerbated EAE, suggesting that TRAIL may be inhibiting autoimmune inflammation in the CNS [18]. This evidence concerns the gene TNFSF10 and experimental autoimmune encephalomyelitis.