CLDN23 and endometriosis: According to MSigDB, genes such as C2, CLDN23, and POLR2A were involved in gene signatures including allograft rejection, coagulation, complement, and DNA repair, suggesting a pro-inflammatory epithelial microenvironment with potential genomic instability processes that have been extensively reviewed and proposed as mediators of endometriosis [68], as well as potential promoters of carcinogenic progression [69,70].