While they differ in that adenomas from the ApcMin/+ model lack functional Apc whereas those from AOM/DSS-treated mice retain wild-type Apc and its chromatin-associated functions, loss of the Apc-dependent cytoplasmic mechanism promoting β-catenin degradation is a common feature of both adenoma types that makes them useful for the identification of canonical Wnt target genes. This evidence concerns the gene APC and adenoma.