Since the coexistence of AChE or BChE with Aβ aggregates in senile plaques (SPs) can accelerate Aβ aggregation, thereby exacerbating neurotoxicity [31,32,33], ChE inhibitors have emerged as promising targets for AD treatment, leading to the development of FDA-approved drugs for AD treatment, such as donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) (Figure 1) [27]. The gene discussed is ACHE; the disease is Alzheimer disease.