We found that changes in β‐catenin expression in samples of NASH‐driven HCC were positively correlated with FGF9 expression; in addition, our results showed that FGF9 promotes increased β‐catenin stability in NASH‐driven HCC by regulating the ERK1/2‐GSK‐3β signaling pathway. Here, GSK3B is linked to metabolic dysfunction-associated steatohepatitis.