The authors suggested that this BP increase may be due to deregulated eNOS (endothelial nitric oxide synthase) activity and increased angiotensin II–AT1R signaling, since there was a reduction in endothelium-derived NO production, which, when compromised, could lead to the development of CVDs, such as hypertension [28,29]. The gene discussed is AGTR1; the disease is hypertensive disorder.