Interestingly, HBV infection and the activity of the TGF-β-miR-34a-CCL22 axis predispose HCC patients to the development of PVTT, possibly through the formation of an immune-supportive microenvironment that favors the colonization of disseminated HCC cells in the portal venous system [72]. This evidence concerns the gene CCL22 and hepatocellular carcinoma.