provided in vivo insights that validate the role of CAFs in promoting HCC progression through the recruitment of MDSCs via the fibroblast activation protein (FAP)-orchestrated urokinase-type plasminogen activator/receptor (uPAR)/focal adhesion kinase (FAK)/Src/Janus kinase 2 (JAK2) axis, which then activates STAT3 and triggers the expression of C-C motif chemokine ligand 2 (CCL2), thereby highlighting the vital importance of CAFs in the development of an immunosuppressive TME (66, 67). This evidence concerns the gene STAT3 and hepatocellular carcinoma.