The cellular and molecular mechanisms involving ERα and, more modestly, GPER in E2 induction of the activity of the AMH promoter (19) and of Sertoli cell proliferation (91) provide biological plausibility to explain the increase in serum AMH levels observed in patients with androgen insensitivity (50, 84) or with Peutz-Jeghers syndrome (46). The gene discussed is AMH; the disease is Peutz-Jeghers syndrome.