AKT1 and Sepsis: Accumulating evidence suggests that the cross-talking of JAK2/STAT3 (p-JAK2 and phospho-Tyr705) with other pathways such as NF-κB (p-IKKα/β, p-IκBα and p-P65), MAPK (p-JNK, pJun, p-P38 and p-ERK1/2), AKT (p-AKT), TLR4, mediate hyperinflammatory factor production during sepsis [40,42].