SAA is produced and secreted by the liver as well as adipose tissue [41] and SAA directly participates in several processes that contribute to atherosclerosis (e.g. increased oxLDL retention time, stimulation of vascular remodeling).[42, 43] Consistent with the observed reduction of SAA and the reduction in VCAM-1, a vascular marker of inflammation, we found reduced atherosclerotic plaque area in mice that were treated with NI. Here, VCAM1 is linked to atherosclerosis.