Similar to our findings, TAGLN silencing inhibited TGFβ1-induced cell migration in lung fibrosis model.6 Interestingly, it has been hypothesized that TGFβ1 released from the bone matrix during bone resorption phase of bone remodeling mediates coupling of bone resorption to bone formation by inducing migration of hMSC to the bone-formation sites.28, 29 It is plausible that the enhanced hMSC motility and migration is achieved through upregulation of TAGLN and may thus have a role in recruiting progenitor cells to the bone-formation sites. This evidence concerns the gene TGFB1 and pulmonary fibrosis.