Since the most important feature of ILD is repeated damage or repair of type II alveolar epithelial cells, Krebs von den Lungen‐6 (KL‐6) secreted by type II alveolar epithelial cells is highly regarded.6, 7 When epithelial cells are damaged, KL‐6 enters the circulation, promotes fibroblast proliferation and migration, inhibits apoptosis, and aggravates the development of pulmonary fibrosis. This evidence concerns the gene MUC1 and pulmonary fibrosis.