Model validation was performed through behavioral assessments, quantification of NMDAR-IgG titers, and immunohistochemical analyses, demonstrating that GluN1-induced autoimmune responses resulted in spatial memory deficits and anxiety-like behaviors, while further confirming the predominant involvement of B cell-mediated mechanisms in anti-NMDAR encephalitis pathogenesis. This evidence concerns the gene GRIN1 and encephalitis.