The classical Nrf2 activator sulforaphane also shows antifibrosis effects on IPF fibroblasts in vitro by reversing the hallmarks of myofibroblastic differentiation (such as the increase of α-SMA, collagen I, fibroblast proliferation, migration, and contraction), even under TGF-β stimulation, and the antifibrosis activity is dependent on the restoration of redox balance by Nrf2 activation. Here, TGFB1 is linked to idiopathic pulmonary fibrosis.