Accumulated evidence suggests that endometriosis in natural and IVF cycles affects human LY2603618 implantation (Arici et al, 1996, Barnhart et al, 2002 and Jacobson et al, 2010). Our group has consistently demonstrated at the clinical level that endometriosis is not detrimental to embryo implantation in ovum recipients (Budak et al, 2007, Diaz et al, 2000 and Simon et al, 1994). Endometrial markers, however, have been reported to be significantly different in eutopic endometrium between women with endometriosis compared with women without endometriosis (May et al., 2011), and further association between altered expression of several markers and impaired embryo implantation of endometrial origin has been proposed in women with endometriosis (Daftary et al, 2002, Lessey et al, 1994, Revel, 2012, Taylor et al, 1999 and Wei et al, 2009). Candidate endometrial markers that have been reported to be disrupted are αvβ3 integrins, methylation of HoxA10 — a known stimulator of αvβ3 expression — glycodelin A, osteopontin, lysophosphatidic acid receptor, hepatocyte growth factor, 17-β-hydroxysteroid dehydrogenase, leukaemia inhibitory factor, matrix metalloproteinases, endometrial bleeding factor or indian hedgehog (Daftary et al, 2002, Lessey et al, 1994, Revel, 2012, Taylor et al, 1999 and Wei et al, 2009). Steroid hormone pathways may also be altered in women with endometriosis. In fact, an up-regulation of oestrogen receptors as well as progesterone resistance status owing to the absence of the beta isoform of its receptor has been described (Lessey et al, 1988 and Wu et al, 2006).