In studies reported here, we have focused on SMAD3 as a key factor in the pathophysiology of CAD, because of its localization in a CAD associated locus [4, 35], its central role as an effector in the TGFβ pathway [36–40], and its function as a transcriptional regulator [30, 39, 41, 42]. This evidence concerns the gene SMAD3 and coronary artery disorder.