While depletion of TGFBR1 using Amhr2-Cre that is only expressed in the mesenchymal compartment of the uterus causes myometrial defects5–7, deletion of Tgfbr1 in the uterine epithelium, stroma, and smooth muscle using progesterone receptor (Pgr)-Cre results in abnormal placental development and metastatic endometrial cancer, which appears to be contingent upon a pregnancy-associated remodeling event of the endometrium30,31. Here, AMHR2 is linked to endometrial cancer.