In high-fat-diet models, dysbiosis–LPS–TLR4/NF-κB activation promotes steatosis and inflammation, creating an HCC-permissive milieu; while no direct 4HHA–CCA/HCC link is reported, gut–liver–immune mechanisms (e.g., biliary epithelial inflammation, angiogenesis) are plausible and testable (12). Here, NFKB1 is linked to steatosis.