This, in conjunction with data showing that co-transfer of Tc17 cells with subpathogenic numbers of CD4+ T cells could induce the disease in mice resistant to EAE and deficient in both IL-17-producing CD4+ T cells and Tc17 cells (154), corroborates the important role of Tc17 cells in EAE/MS pathogenesis. The gene discussed is IL17A; the disease is myeloid sarcoma.