The synthesis of TNF-α by infiltrating M1 macrophages was found to be enhanced by a paracrine interchange with breast cancer epithelial cells [118], and Hagemann et al. [119] showed that culture of an ER-positive human breast cancer cell line with TNF-α-secreting macrophages increased its otherwise poor invasive capacity, an effect that was associated with elevation in the production of matrix metalloproteinases (MMPs), critical for the invasion cascade, and was dependent on increased NF-κB activation. Here, NFKB1 is linked to breast carcinoma.