In vivo, a lack of TGR5 in mice can promote diethylnitrosamine (DEN)-induced hepatocyte death, compensatory proliferation, and the gene expression of certain inflammatory cytokines, matrix metalloproteinasesacute, and liver carcinogenesis to a greater extent than wild-type (WT) mice; in vitro, TGR5 activation strongly inhibited the proliferation and migration of HCC via suppressing STAT3 signaling, and its DNA binding activity [54]. This evidence concerns the gene GPBAR1 and hepatocellular carcinoma.