We conducted a series of experiments, such as gain- and loss-of-function assays, the application of the specific antagonist and agonist of GPR65, and combined with Gpr65-deficient mice as well as mouse bone marrow transplantation (BMT) experiments to investigate the function and the underlying mechanisms of GPR65 in HMs, hepatic stellate cells (HSCs) and hepatocytes (HCs), and the intercellular network during liver fibrogenesis, thus providing a new therapeutic strategy for the prevention of liver fibrosis. This evidence concerns the gene GPR65 and Hepatic fibrosis.