Like most pore-forming toxins, AβO can induce perforation of neuronal and mitochondrial membranes; this is considered a mechanism of neurotoxicity induction and is observed in human AD patients (Lin et al., 2001; Lashuel et al., 2002, 2003; Inoue, 2008; Tong et al., 2018). The gene discussed is ABO; the disease is Alzheimer disease.