Although the current study design does not enable us to determine the exact etiology of the structural impairments identified, the reductions in neural volumes in regions of the brain with high concentrations of glucocorticoid receptors, in areas shown to be affected negatively by increased glucocorticoid exposure in in vivo and murine studies, suggests that the brain abnormalities we describe in patients with CAH relate to chronic excess glucocorticoid exposure. This evidence concerns the gene NR3C1 and congenital adrenal hyperplasia.