Thus, the genetic mechanisms underlying Apc-mediated mammary tumor formation are strikingly similar between the tissue specific conditional knock-out K14-Cre;Apc+/CKO model and the constitutive Apc+/1572T mice: in both cases one allele is completely lost (the germline conditional KO allele in K14-Cre;Apc+/CKO and the somatic loss in Apc+/1572T) whereas the other retains residual β-catenin downregulating activity (the somatic point mutations found in K14-Cre;Apc+/CKO, and the targeted germline mutation in Apc+/1572T). Here, KRT14 is linked to breast cancer.