Currently, AD is treated by acetylcholinesterase (AChE, E.C. 3.1.1.7) inhibitors to restore the physiological levels of acetylcholine (ACh) and the NMDA receptor antagonist, which reduce the excitotoxicity by mitigating the excessive glutamate stimulation of the receptors [23,24]. The gene discussed is ACHE; the disease is Alzheimer disease.