Because the overactivation of GluN2B-containing NMDARs was reported to result in the accumulation of hyperphosphorylated tau in the hippocampus [32], our results indicate a potential link between GluN2B-containing NMDARs and tau phosphorylation in the frontal cortex of mice exposed to 28-day CRS with MEM treatment. The gene discussed is GRIN2B; the disease is congenital rubella syndrome.