Deletionof the SOCS3 gene in hepatocytes promotes the activation of STAT3, the resistance toapoptosis, and an acceleration of proliferation, resulting in enhanced hepatitis-inducedhepatocarcinogenesis (Ogata et al., 2006b).Thus, miR-650-mediated downregulation of SOCS3 expression by B[a]P is generally associatedwith poor clinical outcome, metastasis, and aggressive phenotype of liver cancer. This evidence concerns the gene STAT3 and hepatitis A virus infection.