Our previous work demonstrated a significant decrease of OPA1 protein content in both human and rat heart failure, whereas MFN1/2 surprisingly increased in human heart failure.8 In the current study, OPA1 mutation led to cardiomyopathy without changing the gene and protein level of MFN1/2 (Table S2 and Figure 7). The gene discussed is OPA1; the disease is cardiomyopathy.