It is known that the AT1 receptor transduces responses to Ang II via G protein-coupled and G protein independent pathways [43] and that peptide antagonists of the AT1 receptor can signal exclusively through the G protein independent pathway [44], so it is not unreasonable for AT1 receptor activation to have differential effects on cell proliferation due to differences in the efficiency of these two signaling pathways in cancer cells. The gene discussed is AGTR1; the disease is cancer.