For example, SOD1 mutations in familial ALS have been shown to lead to abnormalities in mitochondrial morphology, both in biopsies and post-mortem tissues of human patients (Sasaki and Iwata, 2007; Sasaki, 2010) and in cellular and mouse models of the disease (Magrane et al., 2009, 2014; Vinsant et al., 2013; Palomo and Manfredi, 2015). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.