Following the above findings, the same research group showed that the inhibition of miR-26a induced mesenchymal markers expression, including vimentin (VIM) and α-SMA following bleomycin instillation (Liang et al., 2014a), confirming that the loss of function of miR-26a could facilitate lung epithelial cells to transform into myofibroblasts and induce pulmonary fibrosis in mice. Here, ACTA1 is linked to pulmonary fibrosis.