There are many hypotheses regarding the pathophysiology of PCOS, including among them ovarian hyperandrogenism, follicles resistant to rupture due to shell thickness, hypersecretion of luteinizing hormone, increased anti-Mullerian hormone (AMH), which is a blocker paracrine factor for follicular development, and hyperinsulinemia (34). The gene discussed is AMH; the disease is polycystic ovary syndrome.