Confirming that the observation is not a cell-specific or virus-specific phenomenon, we found that knockdown of EAP30 also resulted in significant weakening of antiviral defense against HCV infection in hepatoma cells with and without poly(I:C) pre-treatment, enabling higher levels of intracellular HCV RNA replication than in cells transfected with control siRNA (Fig 5B). The gene discussed is SNF8; the disease is hepatocellular carcinoma.