Although the production of reactive oxygen species (ROS) aims to eradicate pathogens, excessive oxidative stress in sepsis leads to cell membrane lipid peroxidation, protein oxidation, mitochondrial damage, inflammation, and increased inducible nitric oxide synthetase (iNOS)-induced NO, apoptosis and necroptosis [14]. The main antioxidant proteins, including superoxide dismutase (SOD), glutathione, catalase, thioredoxin, and peroxiredoxin, regulate the redox balance in the mitochondria [15]. The gene discussed is SOD1; the disease is Sepsis.