Adoptive transfer of salt-exposed DCs primes hypertension in response to a sub-pressor dose of angiotensin II and IsoLG-protein adduct formation is absent in mice lacking the NADPH oxidase and pharmacological scavenging of IsoLGs prevents DC activation, hypertension and end-organ damage [4, 20] (Fig. 2). Here, AGT is linked to hypertensive disorder.