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Systemic signs of inflammation are present in most patients with acute coronary syndromes. 1–3 Inflammation has also been shown to play a key role in the pathogenesis of in-stent restenosis because it promotes neointimal proliferation, the prevailing mechanism of restenosis after stenting. 4, 5 In this study we question whether the intensity of preprocedural inflammatory activation, assessed by measuring C-reactive protein (CRP)(a prototype acute-phase reactant6) in patients with unstable angina undergoing successful coronary artery stenting, can predict the risk of cardiac events at follow-up.