In some breast cancers, aberrantly overexpressed AGTR1 induces both ligand-dependent and ligand-independent NF-κB activation, mediated by CARMA3, Bcl10, and MALT1, driving cancer cell-intrinsic responses that include proliferation, migration and invasion, as well as cancer cell-extrinsic effects to promote tumor angiogenesis through impacting endothelial cells of the tumor microenvironment (33). This evidence concerns the gene AGTR1 and cancer.