G6PD plays a role in the modulation of the inflammatory response in several immune cells. Peripheral mononuclear cells from G6PD-deficient individuals produce lower levels of the pro-inflammatory cytokines, IL-6, and IL-1β, compared with normal individuals [40]. G6PD-deficient granulocytes display a reduced respiratory burst resulting in diminished bactericidal activity and an increased susceptibility to infection [41,42]. G6PD gene and protein expression are increased in macrophages by free fatty acids and lipopolysaccharides (LPS) [43]. Upregulation of the macrophage G6PD gene in adipose tissue of obese mice is associated with increased levels of proinflammatory cytokines, including IL-6, IL-1β, and MCP-1. The prooxidative genes, including NOXs and iNOS, are also increased when accompanied by increased G6PD gene and protein expression. The increased pro-inflammatory cytokines and pro-oxidative genes are downregulated when the NF-κB and MAPK pathways are suppressed as well as if macrophage G6PD is reduced by chemical inhibitors (6-AN, DHEA) or siRNA [43].