There are numerous hypotheses about the development of NFAI including, among others, the contribution of CYP21A2. An elevated 17-OHP response to adrenocorticotrophic hormone (ACTH) administration, which is a characteristic of CAH, has been also observed in approximately half of the subjects with NFAI [13], [14]. This evidence concerns the gene POMC and congenital adrenal hyperplasia.