A large body of evidence suggests that dysregulation of NF-κB, which is triggered and activated by TME and different pro-inflammatory cytokines, including TNF-α, TNF-β, IL-1β, growth factors, hypoxia, and others, leads to further expression and upregulation of pro-inflammatory genes, enzymes, and pro-tumorigenic proteins that may also be involved in cancer pathogenesis and development including in BC [49, 147–150]. This evidence concerns the gene NFKB1 and cancer.