The hypothesis that oxidized LDL (ox-LDL) is neces-sary, if not obligatory, in the development of atherosclerotic lesions was formulated 20 years ago with the seminal observation that uptake of native LDL by macrophages did not result in foam cell formation. In contrast, uptake of ox-LDL via scavenger receptors resulted in the unregulated accumulation of lipid. 1 Since then, multiple studies in experimental animal models have provided firm evidence of an important role of ox-LDL in atherogenesis. However, the role of ox-LDL in the clinical arena has not yet been established. The report in this issue of Circulation by Ehara et al, 2 as well as several other studies, lends support to the idea that the oxidation of LDL is also relevant in humans and continues to move ox-LDL research from the bench to the bedside. 3