They demonstrated that the “non-pathogenic” antibody (aquaporumab) prevents CDC and ADCC in vitro and reduces NMO-like lesions in an in vivo mouse model [9] as well as an ex vivo spinal cord slice model [10], suggesting that preventing the binding of NMO-IgG to AQP4 is a potential therapeutic option [101]. The gene discussed is AQP4; the disease is neuromyelitis optica.