One theory is that the lesser half-life of the endogenous LH surge induced by GnRH agonist, compared with the HCG, induces a shorter and minor secretion of vasoactive elements such as vascular endothelial growth factor (VEGF), which has an important role in the pathophysiology of OHSS (7). The gene discussed is GNRH1; the disease is ovarian hyperstimulation syndrome.