Glucocorticoid remedial hyperaldosteronism occurs due chimeric gene changes where the 5-prime regulatory sequences of CYP11B1 are fused to the coding region of CYP11B2, which results in ectopic expression of aldosterone synthase in the zona fasciculata, resulting in constant stimulation of the mineralocorticoid receptor and subsequent increased ENaC expression and hypokalaemia. This evidence concerns the gene NR3C2 and Hypokalemia.