It’s worth noting that the pathophysiological characteristics of the surgical indication disease itself may produce reverse regulation: endometrial cells in patients with endometriosis show a 2.3-fold upregulation of BRCA1 expression, and this enhanced DNA repair capability may partially offset the carcinogenic effects of estrogen exposure; while abnormal pelvic floor collagen metabolism in patients with uterine prolapse may inhibit breast tumor microenvironment formation by altering stroma-epithelial interactions (59). This evidence concerns the gene BRCA1 and breast neoplasm.