The in vivo mouse model of NMO chosen for the studies here involved a single, stereotaxic injection of a recombinant monoclonal AQP4-IgG and human complement into brain under conditions that produce robust, reproducible NMO pathology with loss of AQP4 and GFAP immunoreactivity, inflammation, complement deposition, and, most importantly, demyelination with minimal axonal loss. This evidence concerns the gene GFAP and neuromyelitis optica.