Indeed, an increasing body of evidence indicates that the PI3K/Akt pathway serves as a critical negative feedback regulator of exaggerated innate immune and toll-like receptor-mediated proinflammatory responses.44–51 Multiple studies44 47–49 52 53 support the role of the PI3K/Akt pathway in limiting inflammation in endotoxemia and sepsis. Here, AKT1 is linked to serum lipopolysaccharide activity.