Together with two previous studies showing that ectopic expression of miR-155 in hepatoma cells mildly inhibited HBV infection by suppressing SOCS1 and subsequently upregulating the expression of several IFN-inducible antiviral genes (13, 14), our current work suggests that miR-155 might act as a positive regulator in miR-155/SOCS1/IFN-γ negative feedback loop of the innate immune system during chronic HBV infection. This evidence concerns the gene IFNG and hepatocellular carcinoma.