These discoveries demonstrate that AQP5 may regulate AQP2 trafficking, possibly by forming heterotetramers with AQP2, and that the impaired apical localization of AQP2 because of abnormal AQP5 expression may contribute to the deterioration of glucosuria-induced polyuria in diabetic patients as well as to the development of hypoosmotic polyuria in Dot1lAC mice [97,109]. This evidence concerns the gene AQP2 and Polyuria.