Crucially, exposure of primary neuron cultures to Aβ leads to increase in Drp1-SNO, excessive mitochondrial fission, impaired energy metabolism, and neuronal cell loss, mimicking what is seen in AD, while the use of a non-nitrosylable Drp1 mutant prevents these detrimental effects (Cho et al., 2009; Wang et al., 2009; Trushina et al., 2012; DuBoff et al., 2013; Joshi et al., 2017; Pérez et al., 2017; Flannery and Trushina, 2019; Oliver and Reddy, 2019). The gene discussed is DNM1L; the disease is Alzheimer disease.