The long-term, organizational effects of E2 exposure are supported by developmental animal studies, which unlike human studies — barring rare genetic diseases such as prenatal exposure to excess androgen in females with Congenital Adrenal Hyperplasia (CAH) or androgen insensitivity syndrome (AIS) where a genetic mutation results in partial or complete absence of androgen receptor activity and hence effectively no exposure to TST — allow us to separate organizational hormone effects from activational effects. Here, AR is linked to androgen insensitivity syndrome.