TGFB1 and pulmonary fibrosis: Moreover, pathway enrichment analysis indicated that the significant pathways of downregulated genes in the vmab-mIL22 treatment group mainly involved focal adhesion, the inflammatory response pathway, P53 signaling, the TGF-β signaling pathway, lung fibrosis, etc. (Figures 6D–F), which indicated that vmab-mIL22 treatment may increase epithelial repair by attenuating the excessive inflammatory response and subsequent collagen deposition.