Activation of TACE results in increased ACE2 shedding from tissue into the circulation.[6] Shedding and hence loss of ACE2 from the tissue is mediated by angiotensin II and results in the pro-inflammatory effects of angiotensin II being unopposed.[6] Certainly in a rabbit model of atherosclerosis, gene silencing of TACE enhanced plaque stability and improved vascular remodelling,[30] possibly via reduced tissue ACE2 shedding. Here, AGT is linked to atherosclerosis.