In order to examine this possibility, we back crossed mtCaMKII mice for five generations into the CD1 background that expresses WT Nnt. The mtCaMKII mice in the C57Bl/6J and CD1 genetic backgrounds exhibited similar left ventricular dilation (Supplementary Fig. 3b), suggesting lack of increased ROS generation in mtCaMKII hearts was not due to loss of Nnt. Thus, in vitro and in vivo data strongly suggested that mtCaMKII cardiomyopathy was not a consequence of elevated ROS. Here, NNT is linked to cardiomyopathy.