Increased ROS levels in tumor cells may also result from tumor-mediated suppression of antioxidant enzymes’ genes expression (superoxide dismutase (SOD), glutathione peroxidase (GP), etc.)[29, 35], or post-translational modifications of the enzymes, exemplified by the acetylation of SOD [27, 36, 37], which confers antioxidant enzymes prooxidant properties. This evidence concerns the gene SOD1 and neoplasm.