Our data showing a role for TGFβ in the increased migratory capacity of HCV infected hepatoma cells, supports a role for HCV in promoting tumor spread rather than a direct role in the oncogenic process per se. We failed to observe any morphological fibroblast features of infected or HCV glycoprotein expressing hepatoma cells, suggesting a partial de-differentiation process in vitro. Mazzocca et al. recently reported that inhibition of TGFβ receptor I kinase blocked HCC growth, supporting a rationale for therapeutic targeting of TGFβ signaling in HCV associated HCC [35]. Here, TGFB1 is linked to neoplasm.