Endometriosis is a benign, estrogen-dependent disorder that has multifactorial components presumed in its pathogenesis. The molecular mechanisms underlying endometrial tissue attachment to the peritoneal surface or metaplasia of the mesothelium, and subsequent invasion and establishment of a blood supply and survival of the endometriotic implants, are not well understood. Recent advances in molecular biology and genomics suggest an intrinsic abnormality in the eutopic endometrium of women with endometriosis that predisposes to these processes. These are discussed herein.