The cell lines used in this study represent different molecular subclasses of HCC, such as those with mutant or wild-type CTNNB1. We show that regardless of the mutation status of CTNNB1, AXIN stabilization via inhibition of tankyrases can still effectively inactivate WNT/β-catenin signaling, suggesting that AXIN function may represent a key regulatory node in the WNT/β-catenin signaling cascade. Here, TNKS is linked to hepatocellular carcinoma.