Indeed, infection reduced the level of S-nitroso-glutathione, which is a nitrosothiol that releases NO and mimics the effects of endogenous NO and nitrosylation of protein thiols, which implicates NO-dependent regulation of many enzymes, including glyceraldehyde-3-phosphate dehydrogenase [61] and energy metabolism-related enzymes that are involved in glycolysis, and also interferes in the inflammatory response of macrophages [62]. Here, GAPDH is linked to infection.