Unlike central or nephrogenic diabetes insipidus, SCD‐induced urinary concentration defect is unique, because it is accompanied with a high level of urinary vasopressin, indicative of a high level of circulatory vasopressin (Fig. 1B), and increased protein levels of AQP2, ENaC‐β and possible NKCC2 in the outer medulla, and protein abundance and apical targeting of AQP2 and UTA1 protein abundance in the inner medulla (Figs. 2 and 3). This evidence concerns the gene SCNN1B and diabetes insipidus.