Conversely, overexpression of mitochondrial fusion proteins MFN1 or MFN2 augments mitochondrial fusion and protects HL-1 cells against simulated I/R injury [107], whereas hearts deficient in both MFN1 and MFN2 are also protected against acute myocardial infarction due to impaired mitochondria/sarcoplasmic reticulum tethering [111]. The gene discussed is MFN2; the disease is acute myocardial infarction.