In the setting of inactivation of one Ctnnb1 allele, the inability of Apc inactivation to substantially activate certain key β-catenin/TCF-regulated genes with functions in colon crypt compartmentalization and cell migration (e.g., EphB2 and EphB3) or stem cell fate (e.g., Lgr5 and Msi) is likely to underlie the dramatic abrogation of adenoma formation in CDX2P-CreERT2Apcfl/flCtnnb1fl/+ mice. Here, APC is linked to adenoma.