Alzheimer’s disease (AD), the leading cause of dementia, is characterized by the accumulation of beta-amyloid peptides (Aβ) in senile plaques in the brain of affected patients.1 Many cellular mechanisms are thought to play important roles in the development and progression of AD pathogenesis, but Aβ deposit-induced toxicity is still considered to be one of, if not the most, important factors in the pathogenesis of AD.2 Several lines of evidence support the Aβ channel/pore hypothesis stating that Aβ is able to disrupt membranes by causing pore formation.3–6. The gene discussed is APP; the disease is Alzheimer disease.