Inflammation in the CNS of patients with MS or EAE is known to be primarily mediated by T helper type 1 (Th1) (67, 68) and Th17 T-cell (69–71) subsets that produce proinflammatory cytokines, such as TNF-α and IL-17, which have suppressive effects on the T regulatory (Treg) anti-inflammatory T-cell subset. The gene discussed is TNF; the disease is myeloid sarcoma.