One of the most abundant antifibrotic miRNAs is miR-27a, and lentiviral delivery of miR-27a-3p has been reported to reduce BLM-induced pulmonary fibrosis by targeting the phenotypic marker of myofibroblasts, alpha-smooth muscle actin (α-SMA), and two key Smad transcription factors, Smad2 and Smad4 [44]. This evidence concerns the gene ACTA1 and pulmonary fibrosis.