Previous studies have suggested that the maintenance of glomerular endothelial integrity is heavily dependent on the precise regulation of paracrine VEGFA–VEGFR2 signaling between the podocyte and renal endothelium and that anti-VEGF therapy can lead to renal endothelial injury, primarily manifested as proteinuria, hypertension, and renal-specific thrombotic microangiopathy [38,39]. The gene discussed is KDR; the disease is Genetic thrombotic microangiopathy.