2023). Beta‐secretases cleave APP to generate Aβ peptides, which form amyloid plaques and aggravate AD, making their inhibition a therapeutic target (A. M. Silva et al. 2023; Tong et al. 2023). Additionally, the inhibition of AChE, which increases acetylcholine in the synaptic cleft, can help restore cholinergic function compromised in AD, supporting its value as a treatment approach (A. M. Silva et al. 2023; J. Zhang et al. 2024). The gene discussed is ACHE; the disease is Alzheimer disease.