WNT signaling plays an important role in uterine development and function (4–10), and mouse models in which the WNT signaling pathway is activated specifically in the uterus (via loss of APC or expression of a stabilized form of β-catenin) result in uterine defects including myometrial defects, adenomyosis, endometrial hyperplasia, endometrial cancer and infertility (11–14). This evidence concerns the gene APC and endometrial cancer.