Immunofluorescence of lung tissue also showed extensive colocalization of GFP with Grp78, α-SMA, and Collagen I (Fig. 6J), indicating that these supplied exogenous LR-MSC suffered from ER stress and transformed to myofibroblast, which is the likely cause of the failure of treatment for pulmonary fibrosis. This evidence concerns the gene ACTA1 and pulmonary fibrosis.