Since studies have demonstrated that ERS induces apoptosis mainly through IRE1 and PERK signaling by increasing the expression of C/EBP homologous protein (CHOP) and the activation of cleaved proapoptotic factor caspase-3 [12] rather than through ATF6 [13, 14], IRE1 and PERK may be the key signaling pathway regulating the ER stress-apoptosis of T cells during sepsis. This evidence concerns the gene EIF2AK3 and Sepsis.