The ER stress response has been linked to several liver diseases, such as acute liver injury, obesity-associated fatty liver, and viral hepatitis.28, 29, 30 Previous studies from our group and others have reported that GADD34, which is induced by ER stress, dephosphorylated the translational initiation factor eIF2α and recovered from the shut-off of translation.25, 26 Recently, Rao et al.30 documented that CHOP, which is downstream of eIF2α, promotes liver injury and hepatic apoptosis in a GalN/LPS-induced acute liver failure model. This evidence concerns the gene PPP1R15A and animal viral hepatitis.