The Cry-null mice, lacking the core-clock components CRY1 and CRY2 [8], displayed hyperaldosteronism and salt-sensitive hypertension, most likely sustained by the upregulation of the type VI 3β-hydroxyl-steroid dehydrogenase (Hsd3b6), corresponding to the human type I 3β-hydroxyl-steroid dehydrogenase (HSD3B1) gene. This evidence concerns the gene CRY1 and hyperaldosteronism.