Although no single model can replicate the complexity of MS and all its pathogenic pathways [89], preclinical evidences show that blockade of the TRAIL-pathway in mice by various approaches exacerbated EAE, increasing both disease score and the degree of inflammation in the CNS, while treatment with recombinant soluble TRAIL delayed disease onset and reduced the severity of EAE [90, 91]. This evidence concerns the gene TNFSF10 and myeloid sarcoma.