CCL2 and neoplasm: Lastly, CAFs display immunosuppressive properties; CAFs’ pro-inflammatory role, when overexpressing fibroblast activation protein (FAP), could be sustained by CCL2-STAT3 signaling, resulting in inhibited myeloid-derived suppressor cells (MDSCs) infiltration in murine models of cholangiocarcinoma [65], whereas the interaction between CAFs and dendritic cells (DCs) dampens the activation of tumor-infiltrating lymphocytes (TILs) [66].