Our understanding of the role of stem cells in the pathogenesis of vascular disease has been rapidly evolving. It is generally accepted that bone marrow (BM)-derived endothelial progenitor cells (EPCs) participate in arterial repair and angiogenesis after injury by homing to the injured vessel and differentiating into endothelial cells.1 BM-derived cells with smooth muscle cell (SMC)-like phenotype also participate in the pathogenesis of vascular disease.2 Recently, Simper et al.3 reported the existence of smooth muscle progenitor cells (SPCs) in human blood. Hashimoto et al.4 demonstrated the existence of BM-derived progenitors for collagen-producing fibroblasts. Inflammatory cells are clearly mobilized to sites of vascular injury.5 Intriguingly, a recent paper revealed an important role for T cells in hypertension and vascular dysfunction.6 The cytokines that recruit, activate, and promote differentiation of BM-derived vascular cells have been extensively studied and include GM-CSF,7 SDF-1,8 and erythropoietin.9,10 These accumulating data establish a close relationship between BM-derived cells and vascular pathogenesis. However, the role of BM-derived vascular progenitor cells in atherosclerosis remains poorly defined (Figure 1).