Although SOD1 is an important cuproenzymes requiring Cu for full catalytic activity that catalyzes the dismutation of superoxide into molecular oxygen and hydrogen peroxide inactivating EGCG oxidation in vitro [35], the activity of SOD in serum and liver has no significant changes indicating that enhanced EGCG hepatotoxicity induced by Cu–deficiency is not involves SOD in mice. The gene discussed is SOD1; the disease is hyperinsulinemic hypoglycemia, familial, 4.