Of note our study also provided evidence that the aberrant COL1A1 expression in IPF-fibroblasts may involve the FAK/Akt pathway, since both FAKY397 and AktS473 were upregulated in stiff substrata in response to TGF-β1 compared to control fibroblasts, and FAK deletion was sufficient to abrogate the increase in both AktS473 and COL1A1 upon TGF-β1 stimulation. Here, TGFB1 is linked to idiopathic pulmonary fibrosis.