Despite the fact that the murine deletion model of 21-hydroxylase has led to improved understanding of adrenal pathophysiology in CAH (8), it has been difficult to maintain homozygous murine cyp21a2 deletion models (6, 8), making these an unsuitable tool to study systemic effects of 21OHD. This evidence concerns the gene CYP21A2 and congenital adrenal hyperplasia.