Mitochondrial dysfunction has also been observed in SOD1-mutated ALS animal models; an increase in the production of oxidative stressors such as nitric oxide, superoxide, and peroxynitrite, as well as a decrease in the ability of mitochondria to synthesize adenosine triphosphate (ATP) are mitochondrial-based mechanisms causing motor dysfunction [62]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.