POMC and congenital adrenal hyperplasia: DEX is considered to suppress pituitary adrenocorticotropic hormone (ACTH) production in CAH fetuses (5), which subsequently suppresses the fetal Hypothalamic-Pituitary-Adrenal (HPA) axis and prevents the continually increased secretion of adrenal C19 precursors that via both classic and non-classic adrenal steroidogenesis can be converted into androgens and 11-oxygenated androgens (6, 13–18).