Their use is based on the assumption that cholinergic deficitsoccur during the disease and the inhibitors function by increasing the availabilityof synaptic acetylcholine (ACh) by inhibiting its key catalytic enzymes,acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE).3,4 Currently, ChE-Is represent the most promising therapeuticagents and are the only therapeutic class of drugs developed that have producedsignificant cognitive improvement in AD patients.5 In 2003, Trinh et al.6 stated that studies examining AD treatments have focused onreducing cognitive decline by using ChE-Is. The gene discussed is ACHE; the disease is Alzheimer disease.