Based on α1Na,K-ATPase key role in renal Na-reabsorption [5,6] and the role of sodium in hypertension [5] and endothelial stiffness [17,18], the expected functional consequences of lower blood pressure due to lower ATP1A1 expression was demonstrated by lower blood pressure in ATP1A1+/− male mice haploinsufficient for ATP1A1 with 58% reduction in ATP1A1 protein in kidneys. This evidence concerns the gene ATP1A1 and Hypertension.