Our data showed that sepsis induced ER-stress, as determined by the increased phosphorylation of the ER membrane kinase, PERK (PKR-like endoplasmic reticulum kinase) and its substrate (Fig. 6A–C), eIF2α (eukaryotic translation initiation factor 2α) (Fig. 6D–F) and increased the expression of ATF6α (Fig. 6G–I). This evidence concerns the gene EIF2AK3 and Sepsis.