To date, therapeutic options for symptomatic treatment of AD, which include three acetylcholinesterase (AChE) inhibitors (donepezil, rivastigmine, and galantamine) [4] and an N-methyl-d-aspartate receptor (NMDAR) antagonist (memantine) [5], could only result in modest and temporary benefit for memory and cognitive function instead of delaying or stopping the progression of neurodegeneration. The gene discussed is ACHE; the disease is Alzheimer disease.