Then, CTF-η is cleaved by α- and β-secretases to release the long and short Aη peptide, including Aη-α and Aη-β, respectively.6,8 Previous studies have revealed that Aβ deregulates neurotransmitter release from the presynaptic site in both primary neurons and AD model mouse brains.9–11 Aβ directly interacts with cell membranes and membrane receptors to exert its neurotoxic effect and then initiates spine density decrease, synapse loss, and synaptic plasticity impairment,2,12,13 which may lead to neuronal perturbations and memory decline during AD. The gene discussed is LIPH; the disease is Alzheimer disease.