Inflammatory response is triggered when tissues are ex-posed to a variety of insults. This response consists of a cascade of events that includes release of various chemical mediators and recruitment of circulating blood cells (platelets and leukocytes) to the site of injury and their subsequent activation. The inflammatory response attempts to contain the damaging effects of the insult, leading to recovery from its injurious effects. However, when normal checkpoints that limit continuing or ongoing inflammation fail, inflammatory response can become a liability that leads to a diverse group of diseases, including atherosclerosis and thrombosis. A large body of evidence has implicated inflammation in the initiation, progression, and destabilization of atherosclerotic vascular disease, linking many of the known risk factors to atherothrombosis. 1, 2 However, the role of inflammation in other vaso-occlusive disorders, such as neointimal thickening after mechanical injury to arteries during angioplasty and/or stenting, is not as well appreciated. Neointimal thickening after mechanical injury predominantly consists of a fibroproliferative reaction initially involving proliferating smooth muscle cells and later dominated by accumulation of extracellular matrix. Neointimal thickening plays a decisive role in restenosis after stenting because stenting essentially precludes constrictive remodeling, whereas postangioplasty restenosis involves elastic recoil and constrictive or negative vessel wall remodeling (vessel shrinkage) in addition to neointimal thickening. An improved understanding of the molecular mechanisms leading to neointimal thickening after mechanical injury would pave the way for development of novel therapeutic approaches for prevention of restenosis, which has remained the Achilles’ heel of endovascular interventions.