Suppression of β‐catenin signaling in liver is associated with increased apoptosis through unknown mechanisms. Loss of Met, a downstream target of β‐catenin, has been also been shown to induce apoptosis through dissociation of the Met‐Fas complex. We hypothesized that loss of β‐catenin in hepatocytes would exacerbate Fas‐mediated apoptosis. However, we demonstrate that β‐catenin loss paradoxically protects against Fas‐mediated apoptosis. Analysis of mRNA expression levels in wild‐type (WT) and β‐catenin knockout (KO) livers reveals a 9‐fold increase in HGF expression in KO, while baseline levels of Met protein are decreased in KO compared to WT. Expression of Fas protein is modestly increased in KO under unstimulated conditions. We also identify a novel interaction of Fas and β‐catenin in WT livers at baseline, which was dramatically lower in KO. KO and WT mice were next injected intravenously with Jo‐2 antibody (a Fas agonist) and monitored for morbidity. While 100% of WT mice are morbid or dead by 6 hours, 35% of the KO mice were alive and showed a marked reduction in liver injury by histology, serum biochemistry and TUNEL immunohistochemistry. Interestingly, a number of proteins known to be protective against Fas‐mediated apoptosis, such as c‐Jun, heat‐shock proteins and NF‐κB, are basally upregulated in KO livers as assessed by gene array. Thus despite increased HGF mRNA expression and decreased levels of Met protein, we report a decreased susceptibility of β‐catenin KO mice to Fas‐mediated cell death, which appears to be due to the presence of basal chronic injury and apoptosis, which primes the KO livers for protection through upregulation of multiple known anti‐apoptotic factors.