Compound mutant mice with one or both Ahr alleles knocked out (Apcmin/+; Ahr+/− and Apcmin/+; Ahr−/−, respectively) overexpress CTNNB1 and develop cecal tumors at a younger age than Apcmin/+; Ahr+/+ mice, providing additional evidence that AHR acts as a tumor suppressor and downregulates CTNNB1 expression in the intestines. Here, CTNNB1 is linked to neoplasm.