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. The gene discussed is KCNK9; the disease is hyperaldosteronism.