Signaling pathways that activate cellproliferation and invasion are the effectors of HBx, a reverse transcription elementin the HBV genome for fibrosis and oncogenesis, interacted by TGF-β or othertranscriptional factors, such as nuclear factor-κB and Sp-1 (3, –5).Consequently, although HBV replication in infected hepatocytes cannot be eradicated,acting on the HBx-triggered molecular networks and suppressing the cofactors of HBxmight be a potent therapeutic strategy for HBV-infected HCC. The gene discussed is SP1; the disease is hepatocellular carcinoma.