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. This evidence concerns the gene PDE4A and nephrogenic diabetes insipidus.