Further studies have shown that the accumulation of morphologically and functionally abnormal mitochondria induces respiratory dysfunction, which leads to dilated cardiomyopathy in Mfn2-KO mouse embryonic fibroblasts and cardiomyocytes, as well as in Parkin-KO Drosophila heart tubes (103) (Figure 3). This evidence concerns the gene MFN2 and dilated cardiomyopathy.