Fibroblasts exposed to high levels of stiffness have a more profibrotic phenotype and TGFbeta activation is also increased with increased lung stiffness.[37,65] The change in lung mechanics along with recurrent lung injury and resulting activation of the immune system are probable factors in the cyclical activation of pathways resulting in further lung fibrosis. This evidence concerns the gene TGFB1 and pulmonary fibrosis.