The central role of inflammation in atherogenesis has gained broad acceptance and has revolutionized our understanding of this common disease. This recognition has heightened interest in identifying the specific mediators and mechanisms that contribute to the interplay between risk factors (traditional and emerging), inflammation, and the altered biology of the arterial wall that regulates plaque development and complication. 1 In particular, leukocytes have come to occupy center stage as the major cellular effectors of inflammation. When these inflammatory cells join endothelial and smoothmuscle cells in the artery wall, they spur much of the biology that drives atherogenesis and plaque complication.