Overexpression of miR-101 in LL29 (IPF lung fibroblasts) resulted in inhibition of α-SMA, COL1A1, and COL3A1 mRNA and protein expression, while anti-miR-101 increased α-SMA and collagen expression in CCD-8 Lu (normal lung fibroblasts). This evidence concerns the gene ACTA1 and idiopathic pulmonary fibrosis.