The recruitment of monocytes to arterial wall and their transformation into macrophages are generally accepted as important early events in the pathogenesis of atherosclerosis (AS). Our research group found Reticulon3 (RTN3), a member of the reticulon family, may be a candidate pathogenic element in the progress of AS. But it is virtually unknown in which process RTN3 may participate in and regulate the pathogenesis of AS. Here, we hypothesis that RTN3 may participate in the continuous process of circulating monocyte recruitment in AS including: (1) monocyte spreading and adhesion to luminal endothelium; (2) transendothelial migration and may also contribute to the conversion of monocyte to macrophage in subendothelium.