The hypothesis was confirmed by in vivo results showing that the passive transfer in rodents of human anti-NMDA receptor encephalitis patients’ CSF or of human anti-NMDA receptor autoantibodies elicited depression-like behaviors and memory deficits, which recovered following the administration of ephrin-B2 [84,85,86] or of selective NMDA receptor positive allosteric modulators [87]. The gene discussed is EFNB2; the disease is depressive symptom measurement.