It has been reported that the nephrotoxicity induced by GN involves different pathways, including oxidative stress (OS), inflammation, nitric oxide (NO) generation, lipid peroxidation, and decreased efficiency of kidney antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione peroxidase, and reduced glutathione (GSH) levels [21]. This evidence concerns the gene SOD1 and ganglioneuroma.