These clinical and epidemiological observations are supported by a recent review of animal models of preeclampsia (Davis et al., 2012b), including those generated by systemic hypoxia, by mechanical reduction of maternal uterine artery blood flow, in genetically modified animals lacking endothelial nitric oxide synthase (eNOS), or by overexpression of sFlt-1 by infection with adenovirus carrying this protein. Here, NOS3 is linked to preeclampsia.