LHCGR and polycystic ovary syndrome: 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].