A previous study used tandem mass tag (TMT) labeling quantitative proteomics technology to analyze differentially expressed proteins in the lungs of mice with or without exposure to fine particulate matter (PM2.5) and found that the extracellular matrix- (ECM-) receptor interaction, phagosome, and phosphatidylinositol 3-kinase- (PI3K-) protein kinase B (Akt) signaling pathways contribute to PM2.5-induced pulmonary fibrosis [20]. Here, AKT1 is linked to pulmonary fibrosis.