The notion that increased cellular oxidative stress contributes to ALS is supported both by observations from post-mortem ALS tissues, where widespread accumulation of oxidative damage to proteins, lipids, and DNA have been noted [6], and by studies showing that superoxide dismutase (SOD1) mutations are related to increased protein and lipid oxidation [7]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.