Strikingly, recellularizing these IPF ECM scaffolds with normal human lung fibroblasts led to a transforming growth factor β (TGFβ)-independent increase of myofibroblast differentiation and alpha-smooth muscle actin (αSMA) expression, implicating the ECM in facilitating fibrogenesis by directly influencing the biological behavior of fibroblasts. Here, TGFB1 is linked to idiopathic pulmonary fibrosis.