Our findings agree with data that spontaneously forming GCs during autoimmunity depend on IFN-γ and STAT1 signaling32 and that administration or expression of the Th1 cytokines tumor necrosis factor (TNF) and IFN-γ in the subarachnoid space of myelin oligodendrocyte glycoprotein (MOG)-immunized rats induces ELS formation in the meninges, subpial demyelination, and neuronal loss.21 The gene discussed is STAT1; the disease is Autoimmunity.