The condition of tubal ectopic pregnancy is presented from diverse points of view, bringing out physiological explanations for its occurrence in primates and striking absence in other mammals. Part of the flexibility underlying ectopic pregnancy in humans stems from the absence of a uterine luteolytic mechanism, enabling early embryonic development in the Fallopian tube without compromising function of the corpus luteum. Attention is devoted to a potential overlap between the composition of tubal and uterine fluids, and to specific mixing between the two fluid compartments, expressed in an ability of the human oocyte or zygote to tolerate transplantation to the uterus. Perturbed tubal oocyte transport is seen as a contributory factor, not least as a sequel to episodes of infection and a modified endosalpinx, but the essay then reasons strongly for an involvement of endometriosis in the aetiology of tubal ectopic pregnancy. Proliferation of refluxed endometrial tissue arrested within the Fallopian tube could provide the epithelial characteristics of a uterine environment. Accordingly, an experimental model is proposed for tubal ectopic pregnancy in animals based upon transplants of endometrial tissue and the subsequent introduction of embryos into both the Fallopian tubes and uterus; the latter would suppress the luteolytic mechanism. Finally, advances are suggested based upon molecular scanning of human ectopic tissues and those derived from animal models. If molecular probes could be developed to detect either early tubal pregnancy or a propensity to this pathology, such advances would clearly have clinical relevance—not least in view of an enhanced incidence of tubal pregnancy arising after assisted reproduction technology.