The mechanisms behind this process are not clear, but in view of the similarities between individuals with Cushing’s syndrome and those with metabolic syndrome (MetS), it has been proposed that, despite normal levels of circulating cortisol, these phenotypes might arise as a consequence of tissue-specific cortisol excess due to increased activity of the enzyme 11-beta hydroxysteroid dehydrogenase type 1 (HSD11B1) [7]. This evidence concerns the gene HSD11B1 and metabolic syndrome.