The evidence indicates that IFN-γ-producing CD4+ Th1 cells and interleukin (IL)-17-producing CD4+ Th17 cells [8,9] play a crucial role in the pathogenesis of human MS and murine EAE, and suggest that these inflammatory CD4+ T cell subsets co-operate to promote CNS autoimmunity. This evidence concerns the gene IFNG and myeloid sarcoma.