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Brice Bellessort,1 Anne Bachelot,1,2 Virginie Grouthier,2 Camille De Lombares,1 Nicolas Narboux-Neme,1 Paolo Garagnani,3,4 Chiara Pirazzini,3,4 Simonetta Astigiano,5 Luca Mastracci,6,7 Anastasia Fontaine,1 Gladys Alfama,1 Evelyne Duvernois-Berthet,1 Giovanni Levi1 1Evolution of Endocrine Regulations, Department AVIV, National Museum of Natural History, Paris, France; 2AP-HP, Department of Endocrinology and Reproductive Medicine, Reference Center for Rare Endocrine Diseases, Pitié-Salpêtrière Hospital, UPMC, Paris, France; 3Department of Experimental, Diagnostic and Specialty Medicine, Alma Mater Studiorum, University of Bologna, Bologna, Italy; 4Interdepartmental Center “L. Galvani”, University of Bologna, Bologna, Italy; 5Department of Integrated Oncological Therapies, San Martino Hospital, Genova, Italy; 6Department of Experimental Medicine and Center of Excellence for Biomedical Research, University of Genoa, Genova, Italy; 7Division of Anatomic Pathology, Department of Surgical Science and Integrated Diagnostics, University of Genoa, Genova, Italy Background: It has been repetitively shown that the transcription factors DLX5 and DLX6 are drastically downregulated in endometriotic lesions when compared with eutopic endometrium. These findings suggest that regulatory cascades involving DLX5/6 might be at the origin of endometriosis symptoms such as chronic pelvic pain (CPP). We have shown that inactivation of Dlx5 and Dlx5/6 in the mouse uterus results in an endometrial phenotype reminiscent of endometriosis. Methods: We focused on genes that present a similar deregulation in endometriosis and in Dlx5/6-null mice in search of new endometriosis targets. Results: We confirmed a strong reduction of DLX5 expression in endometriosis implants. We identified a signature of 30 genes similarly deregulated in human endometriosis implants and in Dlx5/6-null mouse uteri, reinforcing the notion that the downregulation of Dlx5