Administration of angII in rodent models revealed that disturbances in NADPH oxidase-dependent reactive oxygen species, recruitment of T-cells, development of atherosclerosis, and remodeling of the extracellular matrix all contribute to the effects of angII, eventually leading to vascular stiffening (Landmesser et al., 2002; Wang and Fitch, 2004; Zhao et al., 2004; Guzik et al., 2007). This evidence concerns the gene AGT and atherosclerosis.