The authors previously generated the hypothesis that not only systemic hyperprolactinaemia, but also enhanced local prolactin-mediated signalling in endometriotic lesions, might contribute to the development of endometriosis [38], and concluded that prolactin receptor blockade completely inhibited endometriosis in this mouse model to the same extent as the anti-oestrogen faslodex or the GnRH antagonist cetrorelix. This evidence concerns the gene PRLR and endometriosis.