Hu et al. demonstrated that CAV1 interacts directly with succinate dehydrogenase subunit A, promoting its ubiquitination and proteasomal degradation, causing mitochondrial dysfunction and mitochondria-derived apoptosis in DCM; however, silencing CAV1 reduces apoptosis and improves mitochondrial function 12. Here, CAV1 is linked to familial dilated cardiomyopathy.