Moreover, these results support the proposal (17, 18, 19, 20, 21, 22, 23) that an increased level of oxidative damage of SOD1, triggered by age, may be a key element in ALS development, with SOD1 mutations linked to familial ALS being only an additional factor making the protein more likely to become cytotoxic and increasing the probability of an early onset of the disease. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.