Finally, it should be noted that this new PAMH mouse model suggests that the maternal hyperandrogenisation observed in PCOS is the result of a central action of AMH on GnRH (and LH) contributing to an increase in ovarian steroidogenesis and an inhibition of placental aromatase expression, leading to an increase in testosterone bioavailability (66). The gene discussed is GNRH1; the disease is polycystic ovary syndrome.