In the process of atherosclerosis, increased apoptosis of vascular endothelial cells may destruct endothelial integrity and permit pro-inflammatory cells to migrate into the arterial wall.3 In this study, we first examined the apoptotic status of HAECs in vitro by TUNEL after stimulation of oxLDL, and found that oxLDL increased the number of apoptotic HAECs, whereas NPRC knockdown in HAECs effectively attenuated apoptosis induced by oxLDL (Fig. 5a, b). This evidence concerns the gene NPR3 and atherosclerosis.