PDE1A and nephrogenic diabetes insipidus: Since PDE4D controls a cAMP pool that regulates the expression, phosphorylation and translocation of AQP2 to the apical membrane of the collecting duct principal cells [18] and constitutive activation of PDE4 was found to be responsible for a mouse model of nephrogenic diabetes insipidus [19], we wondered whether the increased activity of PDE4 in the kidneys of the Pde1a mutants could be responsible for the mild concentration defect observed in these mice.