Roy et al. took it one step further and compared the potential placement of multiple forms of human amniotic membranes (AM) in a post-myocardial infarction (post-MI) BALB/c mouse model: native, decellularized (dAM) via lysis buffer and sodium dodecyl sulfate (SDS) or treated with TGF-β to induce epithelial-to-mesenchymal transition (EMT) in amniotic epithelial cells (39). This evidence concerns the gene TGFB1 and myocardial infarction.