Abstract: Alcoholic liver disease is a progressive liver disease caused by long-term excessive alcohol consumption. Its pathophysiological mechanisms are complex, involving the interaction of multiple molecular pathways, such as enhanced oxidative stress, lipid metabolism disorders, activation of chronic inflammatory responses, and endoplasmic reticulum stress. In recent years, the regulatory role of glutathioneS-transferase A1 and the endoplasmic reticulum stress axis in alcoholic liver disease has received widespread attention. The endoplasmic reticulum stress pathway is activated in alcoholic liver disease, leading to protein misfolding, release of inflammatory factors, and apoptosis, thereby exacerbating liver injury. As an antioxidant enzyme, glutathione S-transferase A1 can regulate endoplasmic reticulum stress-related signaling pathways and alleviate endoplasmic reticulum stress-mediated cellular stress responses. In-depth exploration of the molecular mechanisms of glutathione S-transferase A1 and the endoplasmic reticulum stress axis not only helps to elucidate the pathogenesis of alcoholic liver disease but also may provide new theoretical bases and potential therapeutic targets for the early diagnosis and development of targeted intervention strategies for this disease.