“…In this investigation, we identified enriched genes in GO terms and signaling pathways that might be utilized as diagnostic and/or therapeutic targets in endometriosis. Signaling pathways include extracellular matrix organization [101], nervous system development [102], signal transduction [103], hemostasis [104], muscle contraction [105], signaling by retinoic acid [106] and diseases of glycosylation [107] were responsible for advancement of endometriosis. Altered expression of L1CAM [108], HSD17B2 [109], VCAM1 [110], SOX6 [111], FGF10 [112], MMP12 [113], CCR1 [114], PROK1 [115], PRL (prolactin) [116], TIMP3 [117], ADAMTS9 [118], NDNF (neuron derived neurotrophic factor) [119], LHCGR (luteinizing hormone/choriogonadotropin receptor) [120], PDGFB (platelet derived growth factor subunit B) [121], LDLR (low density lipoprotein receptor) [122], CD4 [123], FOXL2 [124], TRPA1 [125], ADRB2 [126], PLAU (plasminogen activator, urokinase) [127], EPCAM (epithelial cell adhesion molecule) [128], UCN2 [129], CYP1A1 [130], NTN1 [131], IL15 [132], BMP2 [133], APOE (apolipoprotein E) [134], CASP1 [135], ABCG2 [136], ACE (angiotensin I converting enzyme) [137], PGR (progesterone receptor) [138], ALPP (alkaline phosphatase, placental) [139], LPAR4 [140], ATRNL1 [141], HLA-C [142], MMP3 [143], PDLIM3 [144], NFASC (neurofascin) [145], IL33 [146], NGF (nerve growth factor) [147], COMP (cartilage oligomeric matrix protein) [148], FST (follistatin) [149], EFEMP1 [150], GATA6 [151], TCF21 [152], PTGS2 [153], HOXC8 [154], AKR1C3 [155], BDNF (brain derived neurotrophic factor) [119], EPHA3 [156], INHBA (inhibin subunit beta A) [157], RAP1GAP [158], TLR3 [159], NOX4 [160], TGFBI (transforming growth factor beta induced) [161], IGF2B...…”