Objective-To evaluate whether a p38␣/ mitogen-activated protein kinase inhibitor, SB-681323, would limit the elevation of an inflammatory marker, high-sensitivity C-reactive protein (hsCRP), after a percutaneous coronary intervention (PCI). Methods and Results-Coronary artery stents provide benefit by maintaining lumen patency but may incur vascular trauma and inflammation, leading to myocardial damage. A key mediator for such stress signaling is p38 mitogen-activated protein kinase. Patients with angiographically documented coronary artery disease receiving stable statin therapy and about to undergo PCI were randomly selected to receive SB-681323, 7.5 mg (nϭ46), or placebo (nϭ46) Key Words: angina pectoris Ⅲ atherosclerosis Ⅲ ischemia Ⅲ stent Ⅲ vascular biology Ⅲ inflammation P ercutaneous coronary intervention (PCI) has become the predominant form of coronary artery revascularization. 1 The benefits for resolution of chronic angina and/or salvation of ischemic myocardium during acute coronary syndromes are well documented. 2 However, PCI procedures can also injure the vessel wall, generating a considerable inflammatory response and smooth muscle cell proliferation, 3,4 culminating in restenosis at the lesion site (observed in 5% to 10% of subjects during the first year after PCI). 5,6