Considering our findings, that active, phosphorylated CaMKII was decreased in HBV replicating cells (Figure 1), and that phosphorylated CaMKII and AMPK levels tend to be lower in tumor than in non-tumor tissue of patients with HBV-mediated HCC (Figure 2), we examined the phosphorylation of mTOR, S6K1, and 4EBP1 in HBV replicating cells (Figure 3). This evidence concerns the gene RPS6KB1 and hepatocellular carcinoma.