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Unlike skeletal or cardiac muscle cells, which are terminally differentiated, vascular smooth muscle (Sm) cells (SMCs [VSMCs]) retain a re-markable degree of plasticity throughout their lives. They can switch between a quiescent con-tractile state and phenotypes of increased pro-liferation, migration, and synthetic capacity (Owens, 1995). Dedifferentiation and rediffer-entiation of VSMCs are believed to be involved in vascular remodeling processes that physiologi-cally enable vascular development and repair, as well as adaptation to chronically altered he-modynamics. However, dysregulation of VSMC plasticity also plays a role in the pathogenesis of vascular diseases such as atherosclerosis, re-stenosis after percutaneous interventions, and systemic as well as pulmonary hypertension (Owens et al., 2004). The differentiation state of VSMCs is under the control of transcriptional regulators. Many genes involved in the regulation of SMC contractility are controlled by serum response factor (SRF), a widely expressed transcription factor which is believed to play a key role in the regulation of Sm differentiation (Miano et al., 2007; Owens, 2007). However, SRF can also induce the transcription of growth-related genes involved in Sm proliferation and dedifferentia-tion, and it is now well established that two families of transcriptional cofactors, the myocar-din family (Pipes et al., 2006; Parmacek, 2007) and the ternary complex factor (TCF) family of Ets domain proteins (Treisman, 1994), differ-entially modulate the transcription of these dis-tinct SRF target genes through their mutually exclusive binding to SRF (Wang et al., 2004). Whereas coactivators of the myocardin family