Van den Berghe and co-workers showed that cortisol levels in sepsis depend on corticotropin-driven adrenal secretion only in the hyperacute phase, thereafter more on delayed cortisol degradation, an increased volume of distribution, and the extent of peripheral metabolism, i.e., inactivation to cortisone or reactivation from cortisone via 11 beta-hydroxysteroid dehydrogenase (11β-HSD) [3, 5–10]. The gene discussed is POMC; the disease is Sepsis.