Interestingly, mice with cardiac-specific deletion (Trx2-cKO) develop dilated cardiomyopathy [23], while mice over-expressing Trx2 attenuated AngII-induced vascular dysfunction and hypertension [24], improved aortic endothelial cells(EC) function, and reduced atherosclerotic lesions at aortic roots [25]. Here, TXN2 is linked to dilated cardiomyopathy.