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Pathophysiology of deeply infiltrating endometriosis remains controversial whereas physiopathologic mechanism of superficial endometriosis is nearly demonstrated. Superficial peritoneal implants derive from adhesion and proliferation of endometrial cells regurgitated in peritoneum with retrograde menstruation. Peritoneal inflammation involving cytokines as TNFalpha and aromatase over-expression might be involved in the endometriosis invasion processus. Specific molecular defects of both eutopic and ectopic endometrium have been identified for each of the processes involved in the disease development. Aromatase inhibitors decrease endometriosis lesions in a mouse model of endometriosis which was induced surgically. Few studies report efficacy of aromatase inhibitors in human endometriosis. Theoretically, aromatase inhibitors should not be used alone in premenopausal women because of the resultant increase in gonadotropin levels. Nevertheless, in premenopausal women, aromatase inhibitors may be used in association with Gn-RH agonists. TNFalpha is a secretory factor of macrophages that is known to be increased in the peritoneal fluid of women with endometriosis. Granulosa cells from these women produce higher levels of TNFalpha. This cytokine can stimulate adhesion and proliferation of endometrial cells and enhances metalloproteasis expression, making thus endometrial cell invasion easier. It also stimulates angiogenesis by regulating expression of IL-8. TNFalpha is also cytotoxic to gametes. In mice and baboon models with induced endometriosis, anti-TNFalpha (TNF binding protein-1) decreases AFS score stage and reduces in size the endometriotic foci. No clinical assay has studied TNFalpha efficacy on human endometriosis.