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). The gene discussed is COL3A1; the disease is idiopathic pulmonary fibrosis.