However, it is well known that the TWEAK/Fn14 axis affects the immune response upon tissue injury [4] and it has been hypothesized that it induces the recruiting of proinflammatory mediators during the acute phase of MI while at later time points, it participates in extracellular matrix remodeling and fibrosis. This evidence concerns the gene TNFRSF12A and myocardial infarction.