Activation of the renin–angiotensin aldosterone pathway has been shown to augment pathways leading to an optimal tumor growth environment via proinflammatory, proangiogenic, and apoptotic signaling pathways involving angiotensin II, transforming growth factor-β, epidermal growth factor, vascular endothelial growth factor, and tyrosine kinase [6,7]. The gene discussed is REN; the disease is neoplasm.