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). The gene discussed is ATF6; the disease is Sepsis.