Consistently,BNP knockout Dahl salt-sensitive rats present hypertension, in associationwith left ventricular hypertrophy,44 andabnormal function in the heart (i.e., cardiac stiffness, fibrosis,QT interval prolongation, and thrombosis) and the kidneys (i.e., glomerulardamage, proteinuria, and fibrosis).44 Thehuman data revealed that deficiency in BNP activation is observedin the early stage, including pre-hypertension and stage 1 hypertension,45,46 supporting the reports of furin reduction in hypertension. The gene discussed is NPPB; the disease is Hypertension.