In the placenta, the glucocorticoid-inactivating enzyme HSD11B2 converts biologically active cortisol into inactive cortisone, acting as the placental glucocorticoid barrier to protect the fetus from the adverse effects of excessive maternal cortisol [56] and impairment of this placental glucocorticoid barrier is associated with fetal IUGR and development of chronic diseases in later life [57, 58]. Here, HSD11B2 is linked to fetal growth restriction.