Agonists and antagonists of the Ang-(1-7)-Mas axis probably possess a therapeutic potential for the modulation of sodium and water excretion in many physiologic and pathologic renal conditions, such as arterial hypertension, nephrogenic diabetes insipidus, glomerular diseases, chronic kidney disease (CKD), and diabetic nephropathy (see [68–70], for review). This evidence concerns the gene MAS1 and chronic kidney disease.