Ischemic heart disease is a consequence of coronary atherosclerosis. In addition to coronary bypass surgery, a common and often successful treatment is angioplasty, expanding the internal lumen of the coronary artery with a balloon. However, 30% to 50% of angioplasty patients soon develop significant restenosis, a narrowing of the artery through migration and growth of smooth muscle cells. Stents introduced into the coronary artery to keep it open after angioplasty considerably reduce the incidence of restenosis, but 10% to 50% of patients receiving stents still develop restenosis. 1 Recent clinical trials that use local radiation to the treated artery or drugs released by the stent, such as sirolimus and paclitaxel, are reported to improve the clinical outcomes2–5 but may only provide transient protection. Even after these efforts, restenosis remains a major clinical problem in light of the more than 800,000 angioplasty procedures in the United States each year and the generally disappointing results of efforts to prevent restenosis with systemically delivered drugs in humans.