The molecular mechanism underlying the protection associated with oxidative phenotype appears to be NO-mediated enhancement of the antioxidant defense as systemic administration of endotoxin (lipopolysaccharide, LPS) to mimic sepsis led to induced inducible NO synthase (iNOS), CuZnSOD, MnSOD, EcSOD and CAT mRNAs in atrophy resistant oxidative muscle, but not in atrophy prone glycolytic muscle in mice [116]. The gene discussed is NOS2; the disease is Sepsis.