Similar to the effects in gastric normal epithelial cells, in two gastric cancer cell lines, AGS and BGC-823, the secondary bile acid receptor TGR5 was significantly activated after transient DCA stimulation, the expression of p-STAT3 and KLF5 increased stepwise with prolonged recovery time (0–24 h), and activated p-STAT3 mainly accumulated in the nucleus (Figure 4c-e). This evidence concerns the gene STAT3 and gastric cancer.