And to be clear, 5-alpha reductase deficiency is specifically a male intersex condition, or rather a condition affecting male sexual development before birth and during puberty.

This is also one of the conditions for which the concepts of "assigning" both sex and gender at birth actually means something. As in, many affected males are recorded as female at birth and are reared as girls. This is why that terminology exists before it was misappropriated and misconstrued by TQ activists. Males with this condition generally experience most but not all of the hallmarks of male puberty:

With puberty, the affected males have increased muscle mass and deepening of the voice.25 The musculature is noted to be prominent in Dominican, New Guinean, and Turkish subjects.25, 27, 28, 29 Affected males in these kindreds are similar in height to their unaffected siblings, and there is no gynecomastia in adulthood.37, 42 There is substantial growth of the phallus with rugation and hyperpigmentation of the scrotum. Inguinal testes descending into the scrotum at puberty have been observed in some patients.36, 37, 42 Libido is intact, and patients can have erections.25, 43 Although patients are generally oligo- or azoospermic, normal sperm concentrations have been reported in patients with descended testes.44, 45, 46 Affected patients from the Dominican kindred46 and from Sweden47 have been reported to father children, suggesting that DHT does not play a major role in spermatogenesis and sperm function. These clinical findings suggest that pubertal events, including male sexual function and spermatogenesis, are primarily testosterone-mediated (see Table 2).

. . .

The prostate in the affected males is nonpalpable on rectal examination,25, 48 and is rudimentary on transrectal ultrasound and MRI visualization.43, 49 Prostatic volumes are one-tenth the size of normal age-matched controls. DHT replacement therapy results in an increase in prostate size.43, 50 These data provide clinical evidence that prostate differentiation and growth is mediated largely by DHT (see Figure 1 and Table 2). 5α-reductase inhibition as treatment for benign prostate hyperplasia evolved in part from the clinical observation that affected adult males with 5α-reductase-2 deficiency have rudimentary prostates caused by lifelong DHT deficiency. Prostate diseases such as prostate cancer and benign prostate hyperplasia have not been reported in affected subjects with 5α-reductase-2 deficiency.

Affected adult males have less facial and body hair than their unaffected male relatives, and male pattern baldness has never been observed in these subjects.25, 27, 28 The 5α-reductase-2 inhibitor, finasteride, is now used for treatment of male pattern baldness.51, 52

Source. This publication also has some interesting observations about gender identity with respect to males with this condition:

Gender identity is the sense of being male or female, the awareness of knowing one's sex. Gender role is the expression of one's gender identity to the public. It is manifested by one's actions as either male or female.

Affected 46,XY subjects with 5α-reductase-2 deficiency raised as females often change gender role during or after puberty, providing a clinical model for defining the role of testosterone in the evolution of male gender identity. Since our original report in the Dominican community,25, 42, 63, 64 numerous groups have reported gender change in subjects with 5α-reductase-2 deficiency from many countries including individuals from the New Guinea, Turkey, Mexico, Cyprus, Algeria, Italy, Lebanon, Brazil, Pakistan, Saudi Arabia, UAE, Sweden, etc.18, 32, 33 It appears from these published observations that if puberty is permitted to occur spontaneously without surgical and hormonal reinforcement of the female sex of rearing, then a male gender identity, although discordant with the sex of rearing, will prevail. Under these circumstances, it appears that the extent of androgen (i.e. testosterone) exposure of the brain in utero, during the early postnatal period, and at puberty, has more of an effect in determining male gender identity than does sex of rearing and sociocultural influences.42, 64, 65

In the Dominican community, the female sex of rearing was never reinforced through castration and subsequent female hormone therapy. As such, at puberty a change in gender from female to male occurred in the vast majority of subjects from the older generation who were unambiguously reared as females.25, 42, 64 Interviews with affected 46,XY subjects showed that 17 of 18 subjects successfully changed gender identity from female to male. Between 7 and 12 years of age, patients who were raised as girls began to experience considerable anxiety over their lack of breast development and often began to be sexually attracted to girls. They became convinced of their male gender identity over the next several years and were masturbating and experiencing morning erections and nocturnal emissions. The change in gender role occurred on average at 16 years of age, with a range of 14 to 24 years. In three subjects, a gender role change did not occur until they were in their 20s. Admittedly, the fear of being stigmatized and anticipation of harassment by local villagers caused some subjects to hesitate at the prospect of changing gender roles, in some cases until they were confident of their ability to defend themselves.42, 64 We have continued to observe the behavioral characteristics of these subjects for more than 30 years and have no doubts as to their male behavioral pattern in adulthood.

Normally, the sex of rearing and testosterone imprinting of the brain act in unison to determine the complete expression of the male gender; however, subjects with 5α-reductase-2 deficiency demonstrate that in a laissez-faire environment, when rearing (female) is discordant with the testosterone-mediated biological sex, the biological sex prevails if normal testosterone activation of puberty is permitted to occur. From the data, it appears that the extent of testosterone exposure of the brain in utero, in the early postnatal period and at puberty, has greater impact in determining the male gender identity than the female sex of rearing. This experiment of nature emphasizes the importance of androgens, which act as inducers and activators in evolution of male gender identity in man.42, 64, 65

It has been proposed that the gender identity becomes fixed by 18 months to 4 years of age, at the time of language development.66, 67, 68 At this time, a child becomes aware of his or her gender; however, being aware of one’s gender and being unalterably fixed in that gender are two separate issues. The development of gender identity in man is continually evolving throughout childhood, becoming fixed with puberty.

The psychosexual studies in affected subjects with 5α-reductase-2 deficiency demonstrate that in humans, environmental or sociocultural factors are not solely responsible for the formation of a male gender identity; androgens make a strong and definite contribution. These data support the “hormone-influence theory” in the development of gender identity.42, 64, 65