Aiming to understand the regulation of extracellular matrix (ECM) during Trypanosoma cruzi infection, the previous work from our group showed that despite the increase in extracellular matrix observed in vivo, cardiomyocytes and cardiac fibroblasts highly infected with T. cruzi in vitro have low fibronectin expression, even after the exogenous addition of TGF-β and TNF-α to mimic in vivo inflammatory milieu [19,20,21]. The gene discussed is TNF; the disease is Chagas disease.