Research findings examining the effects of mitochondrial ROS scavenging systems on DCM in diabetic mice highlighted the causative role of mitochondrial oxidative stress by partially restoring mitochondrial function, attenuating apoptosis, enhancing cardiomyocyte contractility, and reducing ROS-induced NF-κB-mediated cardiac inflammation [41]. This evidence concerns the gene NFKB1 and familial dilated cardiomyopathy.