There are several other causes of PsA, including enzymatic defects in adrenal steroidogenesis (deficiency of 17α-hydroxylase and 11β-hydroxylase), gain-of-function mutations in the mineralocorticoid receptor (18), saturation of mineralocorticoid receptor binding by cortisol (Cushing syndrome), alterations in 11βHSD2 (syndrome of apparent mineralocorticoid excess), and genetic alterations in sodium channel expression (Liddle syndrome) or the sodium-chloride co-transporter (Gordon syndrome) (19). Here, NR3C2 is linked to apparent mineralocorticoid excess syndrome.