The impetus for this investigation was manifold and included varying roles of NEP substrates/products in the development of hypertension, atherosclerosis, or AAAs; the potential for alterations in systemic AngII concentrations upon NEP inhibition alone; and the possibility of additive or synergistic effectiveness of AT1R antagonism when combined with NEP inhibition in several AngII-induced cardiovascular diseases. The gene discussed is AGT; the disease is Hypertension.