Given that binding of human monoclonal NR1 antibodies to NMDARs is sufficient to cause morphological and electrophysiological changes in neurons resulting from NMDAR down-regulation [16], the presence of cerebrospinal fluid (CSF)-derived NR1 antibodies from patients provides a plausible mechanism for the occurrence of neuropsychiatric symptoms observed in NMDAR encephalitis [56]. This evidence concerns the gene GRIN1 and viral encephalitis.