Clinical studies in MS and studies on a widely accepted animal model of MS, experimental autoimmune encephalomyelitis (EAE), demonstrate that the autoimmune process is primarily mediated by self-reactive Th1 and Th17 CD4+ cells which enter the CNS, where they become reactivated by resident antigen-presenting microglia, recurrently inducing microglial activation and consequent demyelination and axonal loss (McFarland and Martin, 2007). This evidence concerns the gene CD4 and myeloid sarcoma.