Research on preeclampsia has shown that placental dysfunction leads to an alteration of the placental angiogenic balance, characterized by elevated levels of soluble fms-like tyrosine kinase-1 (sFlt-1) and reduced levels of placental growth factor (PlGF).11, 12, 13 sFlt-1 is an antiangiogenic protein that acts by binding and sequestering vascular endothelial growth factor (VEGF) and PlGF, preventing them from interacting with their receptors on the endothelium.14, 15, 16 This results in reduced angiogenesis and impaired placental vascular development.17 The gene discussed is VEGFA; the disease is preeclampsia.