Pre-eclampsia is a multisystemic disorder of pregnancy, affecting more than 5% of pregnancies worldwide annually and is the leading cause of maternal death (1). Clinical diagnosis of this devastating vascular disorder is reliant on long-established but non-specific markers including blood pressure and urinary protein excretion, however, these indicators are prone to operator error and modest test accuracy in recognising women at risk of developing this disorder (2). Correspondingly, at present, no treatment for pre-eclampsia exists other than delivery of the placenta (and hence the baby). This commonly results in iatrogenic prematurity, which, at early gestations is associated with serious complications for the baby as well as considerable health care expenditure, estimated at €45 billion/year. Pre-eclampsia is proposed to result from placental ischaemia induced by a reduction in uteroplacental perfusion, which consequently exposes the placenta to elevated levels of oxidative stress. There is a growing body of evidence indicating that mitochondrial dysfunction acts as a pathogenic mediator of oxidative stress in pre-eclampsia and modulates the clinical characteristics of this syndrome (3,4). The initial aim of DIVINE is to cultivate a method to predict those at risk by combining clinical markers previously identified (5) with serum profiles of both mitochondrial dysfunction/stress and inflammation in women recruited to the Screening for Pregnancy Endpoints (SCOPE) study of low-risk nulliparous women (6). Additionally, DIVINE will aim to develop a novel therapy for pre-eclampsia by directly targeting mitochondrial superoxide scavenging, hence alleviating maternal vascular dysfunction that is evident in this disorder. By combining this novel therapy with an accurate screening test, this research will substantially enhance care provision for this high-risk group and significantly enhance global healthcare savings. Effective treatment of pre-eclampsia will dramatically improve maternal and fetal health worldwide.