Endometriosis is defined as the occurrence of endometrium-like tissue outside the uterine cavity and, histologically, consists of glands and stroma. (1) Such tissue can be found in the peritoneum, ovaries, myometrium, retroperitoneal sites (such as the abdominal wall and rectovaginal septum), and other distant foci. The implantation of retrograde menstrual tissue is the most widely accepted hypothesis proposed to explain the peritoneal and ovarian lesions. (2) However, various hypotheses have been proposed in order to explain the presence of adenomyosis and endometriosis in deep sites and other distant foci. These include uterine hyperperistalsis, metaplastic change of coelomic cells, intravascular spread, and dissemination into scar tissue. (3,4) There is some clinical and laboratory evidence that ectopic endometrial lesions result from dislocation of the basal endometrium. (5) The 63-kDa membrane protein, designated p63, is a homologue of the tumor suppressor gene p53. The p63 protein is expressed in basal squamous cells and subcolumnar reserve cells of the cervix, breast, salivary gland, and prostate. (6) The role of p63 in regulating epithelial proliferation and differentiation has been demonstrated through studies of p63-deficient mice. (7) The p63 protein has been described as a marker of basal and reserve cells in the female genital tract. (8) Staining for p63 is variable and is typically confined to single cells dispersed throughout the eutopic endometrium, including the functionalis layer and the surface epithelium. (9) Staining for p63 has been shown to correlate strongly with altered differentiation, including metaplasia, either in isolation or in combination with endometrial neoplasia. (10) The aim of our study was to determine whether p63 is expressed differently in peritoneal endometriosis, endometriomas, and adenomyosis, as well as in rectovaginal septum and abdominal wall endometriotic nodules of patients submitted to surgery.