In an attempt to understand the mechanisms underlying cardiac fibrosis evidenced in the pathogenesis of Chagas disease, we evaluated the modulation of extracellular matrix components in cardiomyocytes (CM), cardiac fibroblasts (CFs), and L6E9 skeletal myoblasts stimulated with TGF-β, an important mediator of the fibrosis process. This evidence concerns the gene TGFB1 and Chagas disease.