In breast cancer, constitutive activation of NF-κB has been found to be more frequent in TNBC, which can be elicited by both autocrine and paracrine mechanisms, leading to expression of a myriad of downstream targets including inflammatory cytokines, such as interleukin (IL)-6, IL-8, CXCLs and anti-apoptotic genes to confer aggressive growth, stemness and chemoresistance9, 10, 11, 12. This evidence concerns the gene NFKB1 and breast cancer.