Accordingly, ATRA abolished the potential of HBx to stimulate HBV replication in HepG2-NTCP cells, whereas ATRA failed to induce this effect in Hep3B-NTCP cells, suggesting that HBx plays a major role in the p53-dependent inhibition of HBV replication by ATRA in human hepatoma cells. The gene discussed is TP53; the disease is hepatocellular carcinoma.