Restenosis after stent implantation is mainly caused by neointimal proliferation through the stent struts. Experimental studies performed in the last decade indicate that inflammatory mechanisms play a key role in the process of neointimal proliferation and restenosis. Coronary stenting is a strong inflammatory stimulus, and the acute local and systemic inflammatory responses to local inflammation produced by coronary stenting are highly individual and predictive of restenosis and event-free survival. The benefit of anti-inflammatory periprocedural therapy, such as with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) and steroids, and long-term follow-up is dependent on the individual’s inflammatory status. Measurement of acute-phase reactants, such as C-reactive protein plasma concentration, appears to be important for the identification of subjects at high risk and the development of specific treatment tailored to individual patients.