Given dysfunctional TGF-β signaling as a putative genetically-based mechanism for developing PCOS [24], [25], [26], [27], our findings of altered methylation of TGFB3, TGFBR1, KRAS, BMP2, TFE3, Runx3 and Hoxc8, complement previous studies implicating TGF-β superfamily members or their regulators in the pathophysiology of PCOS, including anti-Müllerian hormone (AMH), inhibin B, growth differentiation factor 9, activin A, follistatin, and fibrillin-3 [24], [25], [26], [27], [33], [34], [35]. The gene discussed is AMH; the disease is polycystic ovary syndrome.