The few polyps arising in CDX2P-CreERT2Apcfl/flCtnnb1fl/+ mice were found to have escaped Ctnnb1 targeting, though Cre-mediated somatic inactivation of both Apc alleles occurred in the lesions, likely reflecting strong positive selection for maintenance of wild type Ctnnb1 gene dosage for Apc-mutant colon adenomas to arise and persist. The gene discussed is APC; the disease is colon adenoma.