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She was getting a bit bitter, not about her life or her infertility but toward her family, for their attitude about her condition, their apparent indifference stained dimly with hostility. She knew something was seriously unusual about her case when she was taken as a young teenager to an endocrinologist. The doctor wouldn’t explain anything more to her than her parents had, but he clearly”“found her condition so remarkable that he invited groups of medical residents to examine her while she lay in stirrups, and he never failed to invite outside observers to attend each time she came for a visit. If her twisted ovaries were long gone, what in hell were they looking at up there? Still, she didn’t turn sullen or introverted. She went off to college, spending one year at the all-female Wellesley and three years at the mostly female Vassar. It was the late 1970s, and she embraced feminism. She thrived, academically and socially. She graduated from Vassar at the top of her class. She made throngs of friends. The only thing she didn’t do was lose her virginity. She felt too ashamed of everything below her umbilicus. She didn’t want to think, in any intimate sense, about her missing organs, her amenorrhea, the vagina that had been such”“a source of fascination to so many medical students, and she didn’t want a lover thinking about any of it either. But she didn’t stop dwelling intellectually on her disorder. After graduating from college, she went to law school in Florida. It was during her first year there, while poking around in the medical library, that she found the story of herself. She saw pictures—the kind where the patients’ bodies are shown but the faces are Xed out—and she read descriptions, and she knew the truth immediately and absolutely. She had what was then called testicular feminization and is now more commonly known as androgen insensitivity syndrome, or AIS. This is a fairly rare condition, affecting about one in 20,000 births. But in its rarity it has something to teach all of us, about how to think about the genetics of sex, and about the correspondence between our chromosomes—the readout from a fetal chromosome screen that will tell you, Ta da!, your baby is a girl or a boy—and our brains and our bodies.”“People with AIS do not exist to instruct a benighted world, and some resent being regarded as genetic anomalies that clarify genetic commonness, being the ones in the doctor’s steel stirrups, being the ones whose faces are blotted out in textbooks but whose bodies are naked and available for public scrutiny. Nevertheless, we all need help in learning the obvious, which Jane Carden embodies and which we’ll discuss here and in the next chapter: that women are made, not born; that women are born, not made; and that both statements are true in their profound and limited fashion.   If Jane’s mother had had amniocentesis while pregnant with Jane, and if she wanted to know the sex of the baby, she would have been told, It’s a boy—”“another son in a son-heavy family. And then, when the baby was born, the mother would have been told, Disregard the previous announcement, it’s a girl. Jane has the external genitals of a girl: outer labia, clitoris, and vagina. She has no inner labia, though, and her vagina is short, extending to only about a third the length of a normal vagina. It ends abruptly in a kind of membrane, rather than leading to a cervix that serves as the gatehouse to the womb. She has no uterus or fallopian tubes. She used to have testes in her abdominal cavity, but they herniated noticeably downward into her pelvis and so were removed ten days after her birth. The excised testes were her “twisted ovaries.” Here is what happened to Jane. She has a Y chromosome, in which are embedded a few dozen genes, most of them of as yet undeciphered function. But one gene on the forked-tongue chromosome is quite renowned for initiating the male narrative. It is called SRY, for sex-determining region on the Y”“chromosome. It used to be called TDF, for testes-determining factor, but genes, like syndromes, often go through periodic, inexplicable rehabilitations in which they get new names. In any event, SRY does something rather dramatic when it switches on during the eighth week or so of pregnancy: it starts building testes in a male fetus’s abdominal cavity. Much later in fetal life, those magical little sacs of maleness drop down to the outside of the body, into the scrotum, and later still they paradoxically become pendulous symbols for bravery and strength—He’s got balls!—despite their reputation as the most vulnerable region on a man’s body. In the fetus, the testes bud quickly and begin excreting androgens, hormones such as testosterone. Androgens in turn sculpt the primordial genital buds into a penis and scrotum. But it’s not enough to make a male; at the same time, the”“fetus’s female program must be stifled. To that end, the testes also secrete a hormone called müllerian inhibiting factor, which makes fetal structures that might otherwise develop into a uterus and fallopian tubes wither away. In Jane’s case, much of this action unfolded according to standard operating procedure. Her Y chromosome performed as expected, and SRY switched on. She grew little internal testes. The testes worked. They secreted androgens. They secreted müllerian inhibiting factor. The inhibiting factor prompted the dissolution of Jane’s primordial womb and tubes. But then something happened, or rather didn’t happen. As it turns out, the Y needs the X to complete the creation of Adamically correct genitals. The quintessential female chromosome holds on its grand expanse a surprisingly large piece in the puzzle of man-making. Of its 5,000 genes, one is the gene that allows the body to respond to androgens. It’s not enough to manufacture androgens; the various tissues of the body must be capable of sensing the hormones and reacting accordingly. That requires the contribution of an androgen receptor protein. The tissues of the fetus’s immature genital bud must be dotted with androgen receptor proteins if”“the bud is to respond to androgens and form a penis. And that protein is encoded in the androgen receptor gene, on the X chromosome. Isn’t it romantic? The androgen receptor gene could have been located anywhere in the genome, on any of the twenty-three chromosomes—on chromosome three, say, or number sixteen. But no, it’s on our chromosome, the big fat boring X chromosome. Sheer coincidence, perhaps—although scientists can’t say that for sure*—but still worth a fleeting “hah!” We make females, we make males; if you don’t see what you want in the window, ask for it inside. “Jane Carden had inherited on her X chromosome a mutated, nonworking version of the androgen receptor gene. As a result of the mutation, her body could not respond to the androgens her testes were releasing in considerable abundance, which meant she couldn’t grow a penis or a scrotum. Her body was, and is, androgen insensitive, hence the name of her syndrome. And so, being androgen-deaf, Jane’s body took the course that a mammalian fetus will in the absence of androgens: it chose to go girl. The little knob of her external genitalia became outer labia, clitoris, and a short blind tunnel. The transformation was not complete—no inner labia, and the skin of her vaginal folds is oddly pale, not the usual mauve tone, as Jane puts it, of other white women’s genitals. Still, she is a woman, as much of a woman as I or any menstruating, childbearing female I’ve ever met. With her breasts and rounded hips and comparatively slender neck (to me, one of the biggest giveaways of the”“female body), she can’t help but strike the world as a woman. Most important, she has never doubted her female identity, even as she stood in the medical library, stunned, desperate, reading about her Y chromosome and the testes she had once possessed. There are quirky elements to androgen insensitivity syndrome. The absence of acne and male-pattern baldness: androgens are behind pimples and most cases of thinning hair, in men and women alike. They also stimulate the growth of body hair in both sexes. Jane has no underarm hair and nothing but a downy mist of light baby hair over her pubic region, again for lack of responsiveness to androgens. Some people with the syndrome look like mama mia women, the sort who become actresses and models. Jane had her testes taken out soon after birth and needed to take estrogen replacement therapy at adolescence to fill out her”“female form (and to protect her bones, which are dependent on estrogen). But some women with AIS are not diagnosed until well into adolescence. Their testes didn’t herniate in infancy and nobody had reason to question their chromosomal status. When such girls reach puberty, the testes begin releasing substantial amounts of hormones, mostly androgens but estrogen as well. The hormones travel through the bloodstream to sites like the breast area, where the estrogen acts directly on the tissue. In addition, some of the androgens are converted enzymatically to estrogen. The breasts begin to grow, and grow, and grow, to larger proportions in fact than in most women, for it is a woman’s capacity to respond to androgens that is part of what holds her breast growth in check. (High levels of androgens likewise keep a teenage boy’s chest flat.