Systemic administration of TNF-α in concentrations comparable to those found in the circulation of HF patients has been shown to induce a dilated cardiomyopathy-like phenotype in animal models [95], and cardiac-specific overexpression of TNF-α has been found to promote a phenotype mimicking several features of clinical HF such as cardiac hypertrophy, ventricular dilation and fibrosis, and several biochemical and cellular dysfunctions [96]. This evidence concerns the gene TNF and dilated cardiomyopathy.