Chemical or genetic abrogation of PRCP function perturbs endothelial cell physiology. PRCP loss causes significant elevation of blood pressure as well as increased risk for blood clotting in animal models, most likely because of reduction of genes such as krüppel-like factor 2 and 4 and subsequently, reduced activity of anticoagulant THBD (thrombomodulin) and NOS3 (nitric oxide synthase [eNOS]). This in turn leads to increased production of vascular ROS and uncoupling of eNOS, thereby favoring blood clotting (increased arterial thrombosis [AT]) and blood pressure. This figure is a short version of Figure 7 from the article by Adams et al (page 3929).