Increases in VCAM-1 protein expression as early as 4 weeks (2 weeks post-SAA treatment) and subsequent increased aortic lesion size (at 18 weeks after commencement of SAA treatment) suggest that an acute increase in SAA triggers enhances pro-atherogenic factors that negatively impact the vascular endothelium and translates to accelerated atherosclerosis in these mice in the absence of high-fat loading. Here, SAA2 is linked to atherosclerosis.