In females, anti-Müllerian hormone (AMH) is primarily produced in the ovary to regulate folliculogenesis. However, recent studies have reported the presence of AMH and the AMH type 2 receptor mRNA and protein in the placenta and uterus. We have observed high rates of foetal resorption in the uteri of AMH-overexpressing (Thy1.2-AMHTg/0) female mice, which might indicate that uncontrolled AMH signalling during pregnancy leads to miscarriage. However, we have also observed abnormal embryo development in the Thy1.2-AMHTg/0 mice, which could arise from defects during oogenesis and folliculogenesis. The aim of this study was to determine whether embryos derived from wild-type donor females could be carried to term after embryo-transfer into Thy1.2-AMHTg/0 females. Embryos from wild-type dams were chosen because the oocytes and preimplantation embryos would be exposed to normal AMH levels in the in the ovary and oviduct. Wild-type females were mated with wild-type studs and the embryos were flushed from the uteri and were vitrified at 3.5 days-post coitus. A total of 10 embryos were then transferred into wild-type control or Thy1.2-AMHTg/0 recipient females on day 3.5 of pseudopregnancy. The transfer of embryos into Thy1.2-AMHTg/0 females did not yield a single livebirth compared to livebirth rates of 50% in wild-type control recipients. These findings suggest that elevated levels of AMH during pregnancy can lead to miscarriage and that these effects are independent of the actions of AMH on oogenesis. Research is ongoing to determine the role of endogenous AMH in the uterus and placenta.