Although we strongly suspect that our model could also be applied to patients with other types of feedback-independent ADH release (such as diabetes insipidus or reset osmostat syndrome) and to patients receiving continuous administration of vasopressin analogues (most notably, Intensive Care patients with circulatory shock or patients with severe hyponatremia who are treated with a so-called “desmopressin (DDAVP) clamp strategy” to prevent rapid auto-correction of the plasma sodium concentration), these have not been included in our analysis [4,15]. The gene discussed is AVP; the disease is Hyponatremia.