Since gonadotropin-releasing hormone (GnRH) agonists were developed at that stage, their ability to downregulate pituitary LH and FSH secretion helped increase treatment efficiency.2 However, at the same time, the combination of ovarian stimulation by gonadotropins after GnRH agonist-induced pituitary downregulation and hCG as final oocyte maturation trigger led to a sharp increase in the risk of ovarian hyperstimulation syndrome (OHSS). Here, BRD2 is linked to ovarian hyperstimulation syndrome.