Similarly, the inhibition of Gli but not Smo stimulated an antifibrotic environment and decreased lung fibrosis and lung collagen accumulation [122], whereas Hu et al. showed that Hh signaling, mainly Shh signaling, stimulated myofibroblast differentiation in a Smo- and Gli1-dependent manner and via the Gli1 activation of the α-smooth muscle actin (α-SMA) promoter [118]. Here, SHH is linked to pulmonary fibrosis.