In this study, alismol significantly blocked the increase in GRP78 expression mediated by tunicamycin, whereas it did not affect the levels of CHOP and XBP-1c, suggesting that alismol might represent one of the active components of MEAO responsible for anti-ER stress and hepatic steatosis which might exert a protective effect against ER stress through the inhibition of ATF6-GRP78 pathway among the three branches of UPR. Here, ATF6 is linked to fatty liver disease.