The activation of angiotensin receptor 1 (AT1) by AngII also mediates the development of cardiac and renal fibrosis [2–4] by stimulating synthesis of proinflammatory cytokines, chemokines, adhesion molecules, and growth factors that in turn activate their cognate receptors to promote the proliferation and differentiation of fibroblasts into myofibroblasts that express extracellular matrix (ECM) proteins at high levels [5]. This evidence concerns the gene AGT and renal fibrosis.