Deletions of task1 and task3, respectively, lead to the development of hyperaldosteronism or low-renin hypertension (25–28) In task1−/− mice, hyperaldosteronism was due to aberrant functional zonation of the adrenal cortex, with intense cyp11b2 expression being localized in zona fasciculata instead of the zona glomerulosa. This evidence concerns the gene KCNK9 and hypertensive disorder.