TP53 and hepatocellular carcinoma: Although both HBX3 and hbx2 significantly upregulated ROS levels in Hep3B cells, HBX3 had a higher potential to induce p53-independent ROS generation than hbx2 (Figure 6B), suggesting that the Ser-101 residue in HBx is essential for upregulating ROS levels by enhancing p53 levels and inducing mitochondrial dysfunction in human hepatoma cells.