The goals of this study were three-fold, 1) verify that VEGFA is the main factor contributing to increased ovarian hyperpermeability following hCG-exposure in COS cycles, 2) determine if intravenous administration of a humanized monoclonal antibody targeting VEGFA (Avastin) during COS cycles provided a viable model to interrogate ovarian angiogenesis, and 3) to determine if hCG-induced VEGFA contributes to ovarian hyperpermeability/OHSS symptoms during embryo implantation/early pregnancy. This evidence concerns the gene VEGFA and ovarian hyperstimulation syndrome.