Redox homeostasis mediated by G6PD is implicated in the modulation of the immune response and inflammation. G6PD deficiency is correlated with an increased risk of neonatal sepsis [32–34]. Infants and trauma patients with G6PD deficiency display altered cytokine profiles [35–37]. Glucose overload-induced vascular inflammation in human aortic smooth muscle cells reveals that IL-1β enhances glucose transport and metabolism through the PPP, resulting in an increased pro-inflammatory response, including NF-κB and NOX activation and iNOS protein expression [38]. Blockade of G6PD with either the chemical inhibitor 6-aminonicotinamide, 6-AN, or siRNA against G6PD abolishes the pro-inflammatory response. G6PD deficiency can elevate inflammation through NF-κB-mediated pro-inflammatory cytokine upregulation. An in vitro HepG2 cell model of lipid-induced chronic hepatic inflammation indicates that G6PD knockdown enhances a pro-inflammatory cytokine response and ROS production [39]. Treatment with the anti-oxidative enzyme glutathione peroxidase or the anti-inflammatory agent curcumin in HepG2 cells inhibits the secretion and expression of the pro-inflammatory cytokine IL-8. These findings suggest that G6PD modulates the pro-inflammatory response in an induced and cell-dependent manner.