AKT1 and Sepsis: It has been established that early sepsis is mediated by the pathogenic TLR triggering of TLR-5/-6 while sustained sepsis is most likely mediated through TLR-9 via the activation of P38 MAPK, which has been considered to play a critical role in the release of inflammatory mediators in sepsis and the inactivation of Akt, which is a key negative regulator of the inflammatory response [37].