Additionally, several endometrial molecular alterations have been described during implantation in PCOS: (a) androgen-dependent suppression of glycodelin [137], a cell-adhesion molecule involved in endometrial receptivity [138]; (b) IR-hyperinsulinemia can also diminish glycodelin expression, alongside IGFBP-1, key molecules for endometrial preimplantation maturation [139]; and (c) a hypofibrinolytic state due to increased synthesis of plasminogen activator inhibitor-1 (PAI-1), which has been found to be an independent risk factor for EPL in PCOS [140]. This evidence concerns the gene SERPINE1 and hyperinsulinism.