Copper-zinc superoxide dismutase activity, encoded by SOD1, is expectedly decreased in the SOD1 G93A rat model.81 SOD1, a known contributor to familial ALS, is involved in oxidative resistance and repair gene transcription.82 Thus, when damaged, it is understandable that ROS have been a major area of focus for understanding ALS pathology. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.