The four PCOS phenotypes differ markedly in their clinical, biochemical, and metabolic profiles: hyperandrogenic phenotypes (A–C) generally present with higher serum androgens, insulin resistance, and greater cardiometabolic risk, whereas phenotype D, lacking hyperandrogenism, shows milder metabolic alterations, lower LH/FSH ratio, and better reproductive outcomes, highlighting the heterogeneity of the syndrome [3,4,5,6]. Here, BRD2 is linked to polycystic ovary syndrome.