Indeed in many heart disorders (ischemia/reperfusion, changes of coronary vascular tone, myocardial infarction, LV dysfunction, cardiac hypertrophy, EAD, arrhythmias, or heart failure) prooxidant enzymes and proteins such as NADPH oxidases, Ang II, TNF-α, or monocyte chemotactic protein-1 (MCP-1) are responsible for ROS overproduction. This evidence concerns the gene FMO5 and cardiac hypertrophy.