hCG molecules play a crucial role in the pathogenesis of both forms of OHSS, as they cross-activate follicle-stimulating hormone (FSH) receptor (FSHR)-dependent signals in granulosa cells, inducing the secretion of vasoactive ovarian mediators, such as the vascular endothelial growth factor (VEGF), as well as other growth factors and cytokines responsible for the development of the syndrome [2, 9, 17–21]. The gene discussed is FSHR; the disease is ovarian hyperstimulation syndrome.