In fact, the benefits of direct FGF19 treatment for liver fibrosis have been demonstrated in animal models.[33] Furthermore, treatment with FGF19 analogs also significantly improved liver fibrosis in patients with nonalcoholic steatohepatitis during phase II clinical trials.[34] However, our coculture model data clearly showed that FGF19 released from CRC cells activates HSCs, and this activation can be reversed by infigratinib, suggesting that the activation of HSCs by FGF19 is a specific effect. This evidence concerns the gene FGF19 and Hepatic fibrosis.