Indeed, the protective effects of a synthetic form of rEPO on a mice model of diabetic nephropathy confirm that tubulointersticial fibrosis, triggered by Snail/Smad 3/TGF-β upregulation, leads to EMT as a sequence of the following events: (1) loss of epithelial or endothelial characteristics, (2) α-SMA expression and reorganization of actin fibers, (3) alterations of the basement membrane, and (4) cell migration and replacement of normal resident cells of the interstitium [15, 33]. The gene discussed is ACTA1; the disease is diabetic kidney disease.