While evaluating the effect of the inhibition of β-catenin signaling on BaP metabolism and on the expression and activity of the CYP1 enzymes involved in the bioactivation of BaP, those authors discovered that the suppression of β-catenin in an HCT116-based model of colon carcinoma cells carrying an activating mutation of β-catenin enhances the induction of the expression/activity of enzymes CYP1A1, CYP1A2, and CYP1B1 in HCT116 cells by the genotoxic ligand of AhR: BaP [183]. This evidence concerns the gene AHR and colon carcinoma.