Cardiac-specific overexpression of angiotensin I converting enzyme (ACE), a peptidase that converts angiotensin I to its biologically active counterpart, angiotensin II, in mice, resulted in atrial dilation, fibrosis, and spontaneous AF under free roaming conditions (Xiao et al., 2004), suggesting that increased angiotensin II signaling promotes the development of AF. Here, AGT is linked to atrial fibrillation.