VSMC have been long thought to play a critical role in restenosis by proliferating and migrating from the vessel media to the intima, resulting in intimal hyperplasia. Recently, it has been suggested that the VSMC may play an earlier role in the events leading to restenosis, for example through the production of PDGF. The work described above suggests that the VSMC may mediate both the early inflammatory and thrombotic responses associated with vessel injury. Thus the VSMC may be involved in all phases of vascular injury, including thrombosis, inflammation, and intimal hyperplasia. Additional work will be necessary to fully elucidate the programs activated in VSMC in response to growth and migratory factors. The recent advances in recombinant DNA technology provide the hope that this will lead to novel approaches to attenuate the response of the VSMC to injury.