Excessive mitochondrial fission, driven by Drp1, is a hallmark of AD, leading to β-amyloid precursor protein cleaving enzyme 1 (BACE1) activation and Aβ accumulation in the N2a cell AD model transfected with the mutant β-amyloid precursor protein (AβPP) gene (Reddy et al., 2018). The gene discussed is DNM1L; the disease is Alzheimer disease.