Consistent with the previous finding that miR-200a is a key player in a variety of disease models associated with fibrosis, including pancreatic fibrosis [26], liver cirrhosis [27], and obstructive nephropathy [14], Xu et al. found that miR-200a was down-regulated in TGF-β1-activated pancreatic stellate cells and miR-200a mimic reversed the increased expression of mesenchymal markers vimentin and ECM proteins by activating the PTEN/Akt/mTOR pathway [26]. This evidence concerns the gene MTOR and fibrosis.