Fibroblast activation protein (FAP)-mediated progression of intrahepatic cholangiocarcinoma (ICC) can be abrogated by anti-Gr-1 antibody treatment, as FAP mediates the infiltration of MDSCs in ICC via inducing CCL2 expression to promote tumor progression and angiogenesis [97]. Here, CCL2 is linked to intrahepatic cholangiocarcinoma.