Elevated cortisol levels that can occur due to mifepristone’s mechanism of action [8] can saturate the binding capacity of 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2), leading to increased availability of cortisol to stimulate the mineralocorticoid receptor (MR) and resulting in edema, hypertension, and hypokalemia. Here, NR3C2 is linked to Hypokalemia.