Considering that Hyp treatment in our study upregulated both Mfn1/Mfn2 and Opa1, it is conceivable that strategies aimed at activating mitofusins may complement Opa1-mediated inner membrane fusion to achieve more robust mitochondrial protection in the setting of cardiac ischemia–reperfusion injury. The gene discussed is OPA1; the disease is myocardial ischemia.