In a myocardial infarction murine model, the TNFR1−/− mice showed improved left ventricular contractility and decreased transcript levels of cytokines such as IL-1β, IL-6, TGF-β, and chemotactic protein-1, whereas TNFR2−/− rodents showed an upregulation of TNFR1 and transcript levels of IL-6 and IL-1β in noninfarcted myocardium, accompanied by adverse remodeling and an exacerbation of left ventricular systolic dysfunction [57]. This evidence concerns the gene IL6 and myocardial infarction.