The blockade of steroid conversion results in increased androgen precursors production under corticotropin-releasing hormone-adrenocorticotropic hormone (CRH-ACTH) stimulation, leading to biochemical hyperandrogenism, marked by elevated 17-OHP levels, with variable gravity according to different phenotypes [1,2,4,6,8,9]. Here, CRH is linked to hyperandrogenism.