The pro-fibrotic stimuli lead to an increase in the TGFβ expression level that crosstalks or activates many other downstream pathways (e.g., canonical SMAD3 or non-canonical pathway and growth factors, as listed in the Figure) promoting myofibroblast activation following the aberrant deposition of ECM and progression of IPF. This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.