Although tolvaptan has been shown to induce aquaresis, resulting in an amelioration of hyponatraemia in patients with cirrhosis, congestive heart failure and SIAD 37, 38, 39, 40, to date no direct in vitro evidence has been provided that tolvaptan impairs AQP2 trafficking and insertion to the plasma membrane in collecting duct principal cells in response to vasopressin thus blunting AQP2‐mediated osmotic water permeability. The gene discussed is AQP2; the disease is Cirrhosis.