Strikingly, the overexpression of the HB spliced protein (HBSP) or reverse transcriptase’-RNaseH (RT’-RH) proteins in hepatoma cells, similarly to POL, prevented the nuclear translocation of STAT1 and STAT2 and the activation of STAT1 in response to IFN-α treatment [79,92,93]. This evidence concerns the gene STAT1 and hepatocellular carcinoma.