Its derivation rests on two main pillars, namely the observation that not every degree of urine concentration or AVP release is enough to explain a net EFW gain (contrary to what is often erroneously suggested in clinical guidelines and protocols), and using existing concepts from renal physiology to combine EFW balance and SFW balance and to set the physiological ceilings for the three aforementioned hyponatremia scenarios A–C. The gene discussed is AVP; the disease is Hyponatremia.