This pathogenesis is similar to that of 17 alpha hydroxylase deficiency, which is a CYP17A1 in congenital adrenal hyperplasia (CAH), in which an upstream substrate, corticosterone, accumulates and also acts as a weak glucocorticoid and, sometimes, at very high levels, suppresses ACTH (Figure 1) [6]. This evidence concerns the gene CYP17A1 and congenital adrenal hyperplasia.