In addition to the reported increase in tissue and plasma TNFα concentration in patients with HF and iDCM, cardiac-specific transgenic mice overexpressing TNFα recapitulated the human pathophysiology of DCM with four-chamber dilatation, myocyte hypertrophy, increased fibrosis, diminished β-adrenergic responsiveness, and premature death [57]. This evidence concerns the gene TNF and familial dilated cardiomyopathy.