In humans there are three different isoforms of SODs: human Cu–Zn SOD (SOD1), the mitochondrial MnSOD (SOD2) and the extracellular Cu–Zn SOD (SOD3), and impairment of their antioxidant function or overactivity due to gain of function molecular mechanisms, represents a major pathophysiology role in the development of human neurodegenerative disorders (primarily, Amyotrophic Lateral Sclerosis) and cancer linked to SOD1 abnormalities [1, 2]. Here, SOD2 is linked to amyotrophic lateral sclerosis.