Specifically, the overexpression of HBx in hepatic and hepatoma cell lines activates TLR4 downstream signaling components such as myeloid differentiation primary response 88 (MyD88), IRAK1, and nuclear factor-kappaB (NF-κB), contributing to the secretion of IL-6, a major pro-inflammatory cytokine [25]. This evidence concerns the gene IL6 and hepatocellular carcinoma.