One of the hypotheses is that the shorter half-life of the endogenous LH surge induced by GnRH agonist, compared with the continuous high levels of hCG stimulating the LH receptor, induces a shorter and milder secretion of vasoactive substances such as vascular endothelial growth factor (VEGF) which is known among other proinflammatory cytokines to play a fundamental role in the pathophysiology of OHSS [6], [7]. The gene discussed is GNRH1; the disease is ovarian hyperstimulation syndrome.