Studies have revealed that HBx shifts TGF-β signaling from the TβRI-dependent pSmad3C tumor-suppressive pathway to the JNK-dependent pSmad3L oncogenic pathway during carcinogenesis, as observed in biopsy samples from chronically HBV-infected patients and HBx transgenic mice with liver lesions (26). This evidence concerns the gene TGFB1 and neoplasm.