HBV-HCC pathogenesis involves the deregulation of many cellular signaling pathways including the Wingless-related integration site/Beta-Catenin (WNT/β-CAT), in the Retinoblastoma-Tumor Protein 53 (RB1-TP53) suppressor networks, the Phosphoinositide 3-kinase/mitogen-activated protein kinase (PI3K/MAPK), the Janus kinase/signal transducer (JAK/STAT) pathways and the insulin receptor substrate-1/insulin growth factor (IRS1/IGF) pathways (124–126). The gene discussed is SOAT1; the disease is hepatocellular carcinoma.