Although it is generally believed that most cultured hepatoma cells generally are impaired for poly(I-C)- and virus-activated IFN responses [55], these results are consistent with previous findings that IFN-β promoter activity is more potently induced in HepG2 and Hep3B cells than in Huh7 cells following either liposome-mediated transfection of poly(I-C) or Sendai virus infection [56]. The gene discussed is IFNB1; the disease is hepatocellular carcinoma.