While the data on CAF therapy in liver cancer is still sparse, targeting CAF-specific proteins like fibroblast activation protein, repolarization of the myofibroblastic phenotype, and targeting of CAF-derived signals seems promising.272For example, combination of a CXCR4 inhibitor (receptor for CAF-produced CXCL12) and anti-PD-L1 reduced tumor growth in a mouse pancreatic cancer model,273and combination of TGF-β blockade and PD-L1 antibody therapy increased T cell infiltration into the tumors of immune-excluded mouse breast cancer models.274. This evidence concerns the gene PROS1 and liver cancer.