Importantly, blockade of Drp1 nitrosylation (using the Drp1 (C644A) mutant) prevented A-β-mediated mitochondrial fission, synaptic loss, and neuronal cell death, suggesting that the posttranslational modification (S-nitrosylation) of Drp1 contributes to the pathogenesis of AD. The gene discussed is DNM1L; the disease is Alzheimer disease.