The administration of AMH to pregnant mice led to increased maternal GnRH activity, increased LH and testosterone, and decreased estradiol and progesterone; at the placenta level, AMH treatment induced a decrease in aromatase and 3b-hydroxysteroid dehydrogenase and an increase in LH receptor expression; the female offspring of AMH-treated mice demonstrated an altered GnRH activity and the phenotypic features of PCOS [47]. The gene discussed is CYP19A1; the disease is polycystic ovary syndrome.