Cardiovascular disease is the leading cause of death globally, accounting for over 17 million deaths per year.1 The major underlying cause of lethal cardiovascular events is the sudden occlusion of blood vessels related to atherosclerosis. Over the years, several hypotheses have been proposed to explain the underlying mechanism of atherogenesis, but it is now well established that plasma low-density lipoprotein (LDL) is causatively linked to cardiovascular disease and that subendothelial retention of atherogenic lipoproteins initiates atherogenesis.2–5 Use of both statins and the nonstatin drug ezetimibe has proven that lowering LDL concentrations reduces cardiovascular events in humans.6,7 These drugs are based on the principle that reducing the number of circulating atherogenic lipoproteins decreases the probability that they will enter and be retained in the subendothelium. See accompanying article on page 49 Lipoproteins normally flux into and out of the arterial wall. The transport of LDL across endothelial cells has previously not attracted much attention, but recent studies have shown that SR-BI8 and possibly caveolin-19 mediate LDL transcytosis and that this process is responsive …