Accordingly, normalizing NMDAR dysfunction by enhancing NR1/NR2A while avoiding excitotoxicity due to NR1/NR2B could be a better approach instead of straight NMDAR antagonism, which will impair normal physiological function like memory and cognition, desperately needed in treatment of AD, and induce side effects like apoptosis and psychosis. The gene discussed is GRIN2A; the disease is Alzheimer disease.