Oxidative stress was generated by a mutant superoxide dismutase protein (SOD1-G93A) expression able to cause muscle atrophy by activating autophagy (in particular LC3, a protein that contributes to the formation autophagosome) in SOD1-G93A transgenic mice model of ALS [37,38], suggesting that the modulation of the autophagic process can be a promising therapeutic intervention to counteract muscle atrophy connected with oxidative stress. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.