In animal models, cardiac-specific overexpression of TNF-α is responsible for the development of dilated cardiomyopathy [79], and systemic administration of TNF-α at some plasma concentrations comparable to those found in patients with congestive heart failure (CHF), have been shown to induce a dilated-cardiomyopathy-like phenotype in animal models [80]. This evidence concerns the gene TNF and congestive heart failure.