In support of our theory Cui H, et al. investigated the therapeutic effect of miR-27a on pulmonary fibrosis by demonstrating the inhibitory effect of miR-27a on Smad2 and Smad4, which are the major mediators of the TGF-β signaling pathway; They have shown that α-smooth muscle actin is directly regulated by miR-27a as well, which is the characteristic feature of myofibroblast differentiation28. The gene discussed is TGFB1; the disease is pulmonary fibrosis.