Abnormalities in adducin by genetic mutation have been shown to influence the surface expression and maximum velocity of Na+-K+ ATPase and subsequently faster renal tubular Na reabsorption.[6] Fifty percent of variation in blood pressure between the Milan hypertensive and normotensive rat strains are due to point mutations in the α and β subunits of adducin.[7] Clinical and experimental studies have demonstrated the potential involvement of ADD1 in the pathogenesis of essential hypertension both in human and animals.[8]. The gene discussed is ADD1; the disease is essential hypertension.