Although the increased serum sodium concentrations elicited by lixivaptan administration in patients with euvolemic hyponatremia [17] and in cirrhosis patients with ascites [20] is likely a consequence of an aquaretic effect of lixivaptan, to date no direct in vitro evidence has been provided about the effect of lixivaptan on the vasopressin-induced AQP2 trafficking in collecting duct principal cells. This evidence concerns the gene AQP2 and Hyponatremia.