Preeclampsia (PE) is a devastating complication of pregnancy that puts both mother and child at risk for clinical complications. In severe cases, PE can progress to multi-organ dysfunction and death. Characterized by hypertension (high blood pressure) and proteinuria (protein in the urine), the syndrome occurs in up to 8% of pregnancies. Although it is widely accepted that the pathophysiology of PE involves disturbance of normal blood vessel function in the placenta and the development and function of the placenta, the exact mechanisms underlying PE have not been defined. Discovery of the causal mechanisms in PE is urgently needed so that early assessment of risk and therapeutic interventions can be developed. On page 707 of this issue, Ho et al. (1) report breakthrough insights into the mechanisms of PE. They reveal a central role for ELABELA (ELA), a recently discovered circulating peptide ligand, in placental vascular development and PE in mice.