Previous studies strongly suggested that HBV infection and the activity of the TGF-β-miR-34a-CCL22 axis are important causes for the development of portal vein thrombosis in HCC patients, possibly by creating an immune-subversive microenvironment that favor the colonization of disseminated HCC cells in the portal venous system [25]. This evidence concerns the gene CCL22 and hepatocellular carcinoma.