Abnormal increases in the acetylcholinesterase (AChE) activity in victims lead to low levels of ACh.4,5 The ACh is rapidly hydrolyzed into choline and acetate anions by AChE, which consequently ends the long term excitatory action of neurotransmitters on the postsynaptic membrane.6 The most effective treatment approach to Alzheimer disease is the inhibition of AChE to replenish ACh levels. The gene discussed is ACHE; the disease is Alzheimer disease.