Interestingly, difference to our conclusion herein that FGF9 aggravated the β‐catenin‐mediated accumulation of ECM, it has been previously reported that activation of β‐catenin results from accumulation of ECM and activation of ECM‐related signaling in several types of tumors.[11, 49, 50] Thus, we suggested that a positive feedback loop linking β‐catenin activation and ECM accumulation exists, which could constitute a potential carcinogenic mechanism during the development of NASH‐driven HCC. This evidence concerns the gene FGF9 and metabolic dysfunction-associated steatohepatitis.