Plus ca change, plus c’est la meme chose. It is rapidly closing in on a century since John Sampson’s brace of seminal publications in the mid 1920s concerning the nature and origin of endometriosis and endosalpingiosis. While his terminology and pathogenetic concepts may seem a little quaint by current standards, they were the beginnings of our understanding the derivation of heterotopic endometrial and endosalpingeal tissues, i.e., beyond the anatomical limits in which they were normally found. Thus, local invasion (Sampson’s first category) would correspond to acquired adenomyosis and salpingitis isthmica nodosa. Everywhere else (outside the uterus and fallopian tubes), such ectopic but benign endometrial tissue was ascribed to processes of implantation or metastasis on the one hand or developmental misplacement on the other. Some 20 years later, Goodall added ‘endocervicosis’ to complete the mullerianosis triptych, with local invasion being what we now also think of as deep endocervical glands (deep Nabothian cysts) or cervical endocervicosis and implantation/metastasis equating to peritoneal endocervicosis. There was no proposed developmental misplacement for endocervicosis. Sampson’s original concept of mullerianosis (specifically endometriosis) was of normally sited endometrial tissue with the sometime capacity to transport itself to a variety of ectopic positions by the same mechanisms with which we are familiar in relation to malignant disease and ‘developmentally misplaced endometrial tissue’ was regarded by him as only a theoretical and unsupported pathogenetic possibility. However, others have espoused this latter concept as a valid, if not all-encompassing explanation for ectopic mullerian type tissue, the secondary mullerian system of Lauchlan, a molecular genetic explanation for which is provided by Gaetje et al. It might be only semantics which separates developmentally misplaced tissue of mullerianosis and the mullerian choristoma championed by Batt et al. and of which endocervical examples include lesions reported in the posterior wall of the bladder and small intestine. Endosalpingeal examples would include, but are not limited to, those reported in the appendix and bladder, perhaps also including cystic endosalpingiosis in a variety of intrauterine and extrauterine circumstances and when it occurs in combination with other choristomatous tissues. The parallel concepts of congenital (developmental, ‘embryologically patterned’, choristomatous) and acquired (implantational, metastatic) origins of various forms of