Studies have indicated that silica particles could promote the liberation of copious oxidants and inflammatory factors in macrophages and epithelial cells, which caused a deposition in extracellular matrix, and finally led to pulmonary fibrosis.122 Silica‐induced pulmonary fibrosis, macrophages exposed to silica or fibroblasts exposed to TGF‐β were decreased the miR‐489 level.123 MiR‐489 possesses the anti‐fibrosis action via decreasing MyD88 and Smad3 target. Here, MYD88 is linked to pulmonary fibrosis.