In mice, multiple copies of mutant hSOD1 are required to generate disease-related phenotypes and overexpression of wild-type hSOD1 alleles produced disease-like phenotypes including altered mitochondrial morphology, motor neuron degeneration, ataxia and shortened life span (Graffmo et al., 2013; Jaarsma, 2006; Jaarsma et al., 2000). The gene discussed is SOD1; the disease is cerebellar ataxia.