The clinical manifestation of experimental autoimmune encephalomyelitis (EAE) depends on the initial activation of CD4+ T cells responsive to myelin autoantigens and their differentiation into autoaggressive effector T cells which, when re-isolated from the inflamed central nervous system (CNS) can produce a range of pro-inflammatory cytokines including IFN-γ, IL-17, TNF-α and granulocyte-macrophage colony-stimulating factor (GM-CSF) [1]. The gene discussed is IFNG; the disease is experimental autoimmune encephalomyelitis.