In the context of our review, well-established genetic contributors to PCOS—such as defects in androgen biosynthesis (e.g., CYP11A1, CYP17A1), abnormalities in insulin signaling (e.g., INSR, IRS1), and alterations in gonadotropin receptor function (e.g., FSHR, LHCGR)—were not discussed in detail [12,20,21]. This evidence concerns the gene CYP17A1 and polycystic ovary syndrome.