Recently, Alonso-Herranz and co-workers studied the influence of macrophages on endothelial cells in an MI model, where they showed that MI was associated with matrix metalloproteinase-14 (MMP14, also called membrane type 1 matrix metalloproteinase (MT1-MMP)) production by macrophages, and this could activate latent TGF-β, with Smad2-dependent paracrine effects on endothelial cells and promoting the endothelial-to-mesenchymal transition [99]. The gene discussed is SMAD2; the disease is myocardial infarction.