Based on our passive-transfer mouse model of NMO — established by intracerebral stereotaxic infusion of human autoantibodies to create a focal NMO model (15) — we injected Ctrl-IgG, AQP4-IgG, or AQP4-IgG plus recombinant CHI3L1 into the striatum (Figure 1A), a brain region that frequently exhibits demyelinating pathology associated with motor dysfunction in NMO patients (19, 20). The gene discussed is CHI3L1; the disease is neuromyelitis optica.