Silencing of MARF (mitochondrial assembly regulatory factor – orthologue of mammalian, Mitofusin) and OPA1 in the Drosophila fly heart tube leads to dilated cardiomyopathy, a phenomenon which could be rescued by over-expressing either of the human Mitofusins (MFN1 or MFN2) or superoxide dismutase 1, implicating impaired mitochondrial fusion and oxidative stress in the pathogenesis of the heart failure [176]. This evidence concerns the gene MFN2 and dilated cardiomyopathy.