Although SEM’s primary mechanism is not the inhibition of acetylcholinesterase, there is some evidence to suggest that GLP-1 receptor agonists can reduce the activity of acetylcholinesterase, increasing the availability of acetylcholine in the brain, albeit this effect is less pronounced compared to traditional acetylcholinesterase inhibitors used in AD treatment. The gene discussed is GLP1R; the disease is Alzheimer disease.