Following myocardial infarction (MI), MF proliferate and migrate to the site of ischemic injury and regulate scar formation by reparative and replacement fibrosis; through production of ECM proteins, particularly collagens type I and III and fibronectin [9], and crosslinking of collagen fibres to generate stiffer matrices, which are less compliant to applied forces and more resistant to deformation [8]. This evidence concerns the gene FN1 and myocardial infarction.