NF‐κB activation driven by HBx promotes hepatocyte proliferation, dysregulated apoptosis, and accelerates HCC progression by increasing the expression of proinflammatory cytokines such as IL‐6, IL‐8, and CXCL2, which are crucial in the inflammatory response, and fostering liver fibrosis, thereby creating a microenvironment conducive to HCC transformation [406, 407]. Here, CXCL2 is linked to hepatocellular carcinoma.