ObjectiveThe aim of the present study was to analyze the expression of theCD63,S100A6, andGNB2L1genes, which participate in mechanisms related to the complex pathophysiology of endometriosis.MethodsA case-control study was conducted with 40 women who were diagnosed with endometriosis, and 15 fertile and healthy women. Paired samples of eutopic endometrium and endometriotic lesions (peritoneal and ovarian endometriotic implants) were obtained from the women with endometriosis in the proliferative (n= 20) or secretory phases (n= 20) of the menstrual cycle. As controls, paired endometrial biopsy samples were collected from the healthy women in the proliferative (n= 15) and secretory (n= 15) phases of the same menstrual cycle. We analyzed the expression levels of theCD63,S100A6, andGNB2L1genes by real-time polymerase chain reaction.ResultsAn increase inCD63,S100A6, andGNB2L1gene transcript levels was observed in the ectopic implants compared with the eutopic endometrium of the women with and without endometriosis, regardless of the phase of the menstrual cycle.ConclusionThese findings suggest that theCD63, S100A6, andGNB2L1genes may be involved in the pathogenesis of endometriosis, since they participate in mechanisms such as inhibition of apoptosis, angiogenesis and cell proliferation, which lead to the loss of cell homeostasis in the ectopic endometrium, thus contributing to the implantation and survival of the tissue in the extrauterine environment.