Consistent with the importance of mitochondrial dysfunction and increased ROS/RNS generation in the pathology of alcohol-induced cardiomyopathy and vascular dysfunction we found decreased myocardial mitochondrial function (complex 1, 2 and 4 activities) and increased expression of angiotensin II receptor and its downstream effector ROS generating enzyme NADPH oxidase (gp91 and p22phox isoforms) in young rats exposed to chronic liquid alcohol diet. The gene discussed is FMO5; the disease is cardiomyopathy.