Ghirardini and Segre (1982) [21] have stressed and supported an assumption originally proposed by Schmid Tannwald and Hauser [22] according to it there would be a very strong hyperincretion of Müllerian-inhibiting factor (MIF) in patients with MRKH syndrome, which would cause a failed development of Müllerian ducts as primitive structures (as normally occurs in male phenotype) [23–25], and therefore, they have proposed that MRKH syndrome is considered as one of the slightest forms of pseudohermaphroditism. The gene discussed is AMH; the disease is Mayer-Rokitansky-Küster-Hauser syndrome.