As previously mentioned, ARBs exert their effect on cancer development by blocking AT1R, leaving AT2R unopposed, with a concomitant increase in Ang[1–7] leading to antiangiogenesis, anti-proliferation, and systemic vasodilatation[6] thus eventually reaching an anti-inflammatory state, which explains the possible mechanism by which ARBs reduce cancer development risk. Here, AGTR1 is linked to cancer.