Our in vivo studies demonstrated that, compared with Pla2g7fl/fl silicosis mice, CreLyz2Pla2g7fl/fl silicosis mice presented lower expression levels of cathepsin B. Furthermore, CreLyz2Pla2g7fl/fl silicosis mice treated with an autophagy inhibitor to disrupt autophagic lysosome processes exhibited exacerbated lung fibrosis, mitochondrial damage, and a restored proportion of SiglecFloAMs. The gene discussed is CTSB; the disease is pulmonary fibrosis.