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Hepatocyte death is associated with liver inflammation, fibrosis and hepatocellular carcinoma (HCC). Damaged cells trigger inflammation through activation of Toll‐like receptors (TLRs). Although the role of TLR4 in HCC development has been reported, the role of TLR9 in the development of HCC remains elusive. To investigate the role of TLR4 and TLR9 signaling in liver inflammation‐fibrosis‐cancer axis, we took advantage of mice with hepatic deletion of transforming growth factor‐β‐activated kinase 1 (Tak1ΔHep) that develop spontaneous liver injury, inflammation, fibrosis, and HCC, recapitulating the pathology of human HCC. We generated double knockout mice lacking genes of our interest with hepatic Tak1. Tak1ΔHep mice and Tlr4‐deficient Tak1ΔHep mice had similar serum ALT levels, but Tlr4‐deficient Tak1ΔHep mice exhibited significantly reduced macrophage infiltration, myofibroblast activation and …