In addition, oxidative stress can activate numerous inflammatory mediators, such as adhesion molecules, and proinflammatory cytokine expression (e.g. TNF-α, whose levels are enhanced in anorexia) [37] and immune signaling responses, including phospholipase activity, MAP kinase, and STAT and TLR signaling pathways [38]. This evidence concerns the gene SOAT1 and Anorexia.