Figure 2C shows a significant increase in the levels of transforming growth factor β (TGF-β), β-catenin (CTNNB1), extracellular signal–regulated kinase 1 (MAPK1), c-MYC, mechanistic target of rapamycin (mTOR), and amphiregulin (AREG) in HCC tissue samples, confirming independently the activation of these cancer-related pathways in HCC. This evidence concerns the gene CTNNB1 and hepatocellular carcinoma.