The global impact of ATG5 deficiency on pivotal endothelial homeostatic systems was uncovered by RNAseq and proteomic analysis, and included metabolic changes, activation of p53 (an anti-ROS countermeasure [31]), the UPR pathway (a general mediator of vascular inflammation [32]), and synthesis of prostanoids (regulators of angiogenesis, vascular inflammation and hypertension [33–35]). The gene discussed is TP53; the disease is Hypertension.