Recent advances in our understanding of preeclampsia have centred on the discovery of angiogenic pathway abnormalities in the human placenta. The production of placental sFLT-1 (soluble FMS-like tyrosine kinase 1) or vascular endothelial growth factor receptor 1 (VEGFR1) has been identified and provides a possible serum marker of preeclampsia severity. Importantly, it reflects placental events in early pregnancy in a way that may potentially predict impending preeclampsia. Whether this will be a useful test in very early pregnancy to predict those at risk is yet to be fully determined. The effect of elevated sFLT-1 on circulating VEGF (a decrease) and placental growth factors (PLGF) (a decrease) provides further biological plausibility for a mechanism of placental hypoxia, inflammation and endothelial dysfunction as the central causative pathway in preeclampsia.  How these angiogenic factors specifically target vascular resistance and thus hypertension is not yet known. This pathway has provided novel targets for treatment which are genuinely new. The presence of this “toxic” placental compound has links to the cardinal clinical features of human preeclampsia such as hypertension and proteinuria. These can therefore be the targets for new therapies, i.e. a reduction in proteinuria and a reduction in blood pressure. Ultimately prolonging the pregnancy to a safer time for the baby and mother are goals of treatment. Whether our capacity to control endothelial injury will benefit the mother in terms of long term cardiovascular health is yet to be determined. The capacity now exists to identify interactions with other potential mediators of the hypertensive and endothelial responses such as endothelin 1, nitric oxide synthase, estrogens and the renin-angiotensin system with the ultimate goal of directed and appropriate treatment targets at the right times of an evolving pregnancy.