To summarize, CTLA4 (immune-checkpoint) SNPs and CTLA4-AB treatment, previously associated with autoimmune disease, predispose in humans, as uncovered here, also to NMDAR1-AB, while checkpoint-inhibitor treatment (CTLA4-AB) of healthy adult mice without additional immune stimulation does not further enhance their already high NMDAR1-AB seroprevalence. The gene discussed is GRIN1; the disease is autoimmune disease.