In mice, ELA deficiency leads to hallmarks of PE such as hypertension, proteinuria, glomerular endothelial cell hyperplasia, and low birthweight (i.e., intrauterine growth restriction [IUGR]) [24], making ELA-deficient animals a suitable model for the study of PE, as well as the involvement of ELA in the pathogenesis of PE [84]. This evidence concerns the gene APELA and hypertensive disorder.