The presented study also confirmed that TGF-β is a major inducer of lung fibroblast differentiation to matrix-secreting myofibroblasts, inducing the overexpression of α-SMA and collagen deposition and, indirectly, that Gal-3 is an essential mediator of TGF-β–induced lung fibrosis [26,27]. This evidence concerns the gene ACTA1 and pulmonary fibrosis.