Genetic experimental studies have also long been known to reproduce disease phenotypes (e.g., in mice) that are only a partial approximation of the complex human disease; an example is the Super Oxide Dismutase-1 (SOD1) mutated mouse model for Amyotrophic Lateral Sclerosis (ALS), which has different motor characteristics than the human disease [29]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.