The systemic knockout of mitochondrial fusion proteins OPA1, MFN1, and MFN2 in mice are embryonically lethal [117,118], and the conditional combined deletion of MFN1/2 in adult cardiomyocytes triggers mitochondrial fragmentation, cardiac hypertrophy, and lethal dilated cardiomyopathy [119,120]. The gene discussed is MFN1; the disease is cardiac hypertrophy.