Mice with muscle specific SOD1(G37R) transgenic progressively developed muscular atrophy with myofiber loss and muscle cell apoptosis, microgliosis, neuromuscular junction abnormalities, motoneuron distal axonopathy, and eventually death of motor neurons (Wong and Martin, 2010), indicating that ALS might originate from pathogenesis of skeletal muscle. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.