IN MOST mammalian species, products of the fetal adrenal gland appear to play an important role in regulating maturation of various organ systems in the fetus (1–5), providing the fetus homeostatic mechanisms to respond to stress (6), and initiating and/or participating in the cascade of events culminating in the birth of a newborn (7–9). Thus, cortisol, presumably of fetal adrenal origin, is one of the chemical messengers involved in the stimuli to lung maturation (3,4), deposition of glycogen in the liver (10, 11), and induction of several enzymes in the fetal brain, retina, pancreas, and gastrointestinal tract (12–17) that normally are associated with late intrauterine life. It is well known, from the elegant work of Liggins and colleagues (7), that ablation of the fetal adrenal in sheep prevents parturition, whereas infusion of cortisol or ACTH¹ to the fetus induces premature delivery. Although evidence that the fetal adrenal of the human or nonhuman primate participates in the initiation of labor appears less convincing (5, 8, 18–20), maturation of fetal adrenal steroidogenic enzyme systems that permit de novo synthesis of cortisol (5, 21, 22) must occur, as in sheep (23, 24), to ensure neonatal adrenocortical self-sufficiency in the perinatal period. In addition to these purported roles for fetal adrenal cortisol, it is well established that the fetal adrenal in primates, including the human, is important to the synthesis and secretion of androgen precursors essential to the production of estrogen by the placenta (25–32).