The authors hypothesized that low levels of testosterone in the prenatal period reprograms the hypothalmic–pituitary–gonadal (HPG) axis of the female fetus, resulting in distinct changes of several sex hormone productions such as lower LH relative to FSH, higher SHBG, lower ovarian and serum testosterone, etc., that finally predispose the adult to endometriosis [4,29]. Here, BRD2 is linked to endometriosis.