NF-kB activation in macrophages and ectopic endometrial cells stimulates synthesis of proinflammatory cytokines, generating a positive feedback loop in the NF-kB pathway and promoting endometriotic lesion establishment, maintenance, and development.(28) Because endometriosis is a multifactorial disease, inhibiting NF-kB seems to be a promising strategy for new therapies targeting different cell functions involved in endometriosis development, such as angiogenesis, cell adhesion, invasion, inflammation, proliferation, and apoptosis.(29). Here, NFKB1 is linked to endometriosis.