There is a common ground between heart failure, cirrhosis and nephrotic syndrome with respect to the mechanisms implicated in the development of hyponatremia, namely a state of arterial underfilling which results, as the physiopathological scenario unfolds (see “Basic principles of sodium and water equilibrium”), in an increased release of AVP, an augmented adrenergic drive and the stimulation of the plasma renin angiotensin aldosterone system [12, 46, 198–200]. The gene discussed is REN; the disease is heart failure.