Interestingly, silencing of any constituent of the C10BM complex completely abrogates the angiotensin II-induced NF-κB response and thus blocks cell-intrinsic proliferative and invasive properties, as well as cell-extrinsic effects, such as the stimulation of endothelial cells of the tumor microenvironment to promote tumor angiogenesis [82]. This evidence concerns the gene NFKB1 and neoplasm.