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. This evidence concerns the gene AGTR1 and breast cancer.