In conclusion, as shown in Fig. 7, miR-489 may function as an anti-fibrotic miRNA in silica-induced pulmonary fibrosis by targeting MyD88 and Smad3, and the lncRNA CHRF inhibits miR-489 expression, thus resulting in the activation of inflammation and the fibrotic signaling pathways. This evidence concerns the gene MYD88 and pulmonary fibrosis.