Defective conversion of 17-OHP to 11-deoxycortisol, mediated by 21-hydroxylase (CYP21A2), accounts for more than 90% of the cases of CAH.15-17 Therapy for CYP21A2 deficiency is directed towards providing glucocorticoid in sufficient doses to reduce the excessive corticotropin-releasing hormone (CRH) levels, corticotropin (ACTH) secretion and hyperandrogenemia.18-20 Our patient had the simple virilizing non-salt wasting form of CAH, and after he abandoned his successful glucocorticoid treatment, he presented high serum levels of 17-OHP and infertility. This evidence concerns the gene CRH and polycystic ovary syndrome.