In recent years, it has become increasingly clear that arterial inflammation represents a key feature determining the course of atherogenesis. The consecutive stages in the evolution of atherosclerotic lesions are respectively, plaque buildup and growth, and destabilization, predisposing to plaque rupture and intravascular thrombosis. This chain of events leading from lesion formation to clinical events has been carefully elucidated during the last three decades. C-reactive protein (CRP) has been directly implicated in the pathogenesis of atherosclerosis. In the present review, we will focus on a potentially causal role of CRP during the various stages of atherogenesis.