Considering that both cell types not only release CXCL12 and express CXCR4 but also implement sender and receiver functions for the CXCL12–CXCR4 signaling cascade with its double-edged role in injury-induced restenosis and atherosclerosis, we now sought to analyze the role of the CXCL12–CXCR4 axis in various modes of EPC–SMC interaction including migration, proliferation and phenotype control. The gene discussed is CXCL12; the disease is atherosclerosis.