The results showed that after knocking down the CXCR4, the ability of G-CSF to promote BM-MSC migration to injured tissues and the inhibitory effect of BM-MSCs on pulmonary fibrosis were significantly reduced, further suggesting that G-CSF promotes BM-MSC activity by upregulating the CXCR4 expression. The gene discussed is CSF3; the disease is pulmonary fibrosis.