In addition, OS is promoted by mitochondrial dysfunction: a recent study showed that the downregulation of mitofusin 2 (MFN2) is a key mediator of the defective mitochondrial turnover that characterizes D2CM, while MFN2 overexpression ameliorates DCM by promoting mitochondrial fusion and improving mitochondrial function. This evidence concerns the gene MFN2 and familial dilated cardiomyopathy.