In 1953, the first medical report on Androgen insensitivity syndrome (AIS) was published by J. M. Morris, an American gynecologist. In 1989, the exact location of the human Androgen receptor (AR) gene on Xq11-12 locus was determined and the proof that it is caused by mutations in this gene.

• In 1953, the first medical report on Androgen insensitivity syndrome (AIS) was published by J. M. Morris, an American gynecologist.^{[1][2][3][4][5]}
• Until the late 1950s, Morris’ approach to non-disclosure was consonant with the prevailing medicolegal and ethical climate.^[4]
• In 1988, Minogue and Taraszewski argued that the condition of the patient could not be revealed if the clinician felt that the patient or the patient’s family weren’t in a state to handle the truth about the patient’s condition.^[6][4]
• In 1989, the exact location of the human Androgen receptor (AR) gene on Xq11-12 locus was determined and the proof that it is caused by mutations in this gene.^[7][8][9]
• Until the 1990s, revealing the genotype in CAIS after diagnosis was common. ^[4]
• In 1992, Shah argued that disclosing the genotype is not much relevant to care and as it may be confusing to patient and family.^[4]
• In 1997, Weiner et al expressed his opinion that it was a complex situation whether to tell a patient about her genetic make-up or not as it was questionable topic to deal with. ^[10]

One might fairly call Reifenstein syndrome “even more partial” AIS, but when E.C. Reifenstein described the features of a new syndrome of male “familial hypogonadism” in 1947, it was not known that this condition was due to an abnormal androgen receptor and related to the female conditions of CAIS (complete androgen insensitivity syndrome) or PAIS (partial androgen insensitivity syndrome). Additional familial intersex and hypogonadal conditions described by Lubs, Gilbert, Dreyfus, Rosewater, Walker, and others are now considered variants of the Reifenstein syndrome form of AIS. ^[11]