Utilizing cardiac-specific deletion of Mfn1/Mfn2 and Drp1 to simultaneously eliminate mitochondrial fission and fusion in the hearts of adult mice, researchers revealed that Mfn1/Mfn2/Drp1 cardiac TKO (triple knockout) mice had a longer survival time and developed a unique form of pathological cardiac hypertrophy compared with fusion-defective Mfn1/Mfn2 cKO or fission-defective Drp1 cKO mice, and provided evidence that cardiac pathology was attributed to the imbalance in mitochondrial dynamism (fission and fusion), instead of the absence of either fission or fusion (19). This evidence concerns the gene MFN2 and cardiac hypertrophy.