The silencing of MARF (mitochondrial assembly regulatory factor – ortholog of mammalian, Mitofusin) and OPA1 in the Drosophila fly heart tube causes dilated cardiomyopathy, 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 (Dorn, 2011). The gene discussed is MFN2; the disease is dilated cardiomyopathy.