Thus, because HER2-dependent NF-κB activation underwrites several of the hallmarks of cancer (89), we reasoned that AGTR1 might similarly drive breast cancer progression via an NF-κB-dependent mechanism, and possibly through the same C3BM signaling pathway that we had clearly described as operating in endothelial cells in the context of vascular pathobiology. The gene discussed is AGTR1; the disease is breast carcinoma.