However, given the unique embryonic origin, the singular phenotypic characteristics of coronary artery smooth muscle cells, and the importance of this question in the context of recent GWAS studies linking SMAD3 to CAD risk, we sought to investigate in detail how SMAD3 affects the cell state of HCASMC, and how it might interact at a molecular level with other factors that are involved in the relationship between SMC phenotype and CAD. The gene discussed is SMAD3; the disease is coronary artery disorder.