Herein, we propose that surface ENO1 could play an important role in lung fibrosis based on the following evidence: HL217 has an inhibitory effect on the ENO1/uPAR/plasmin axis, which in turn governs cell trafficking (human PBMC, endothelial cells, lung fibroblasts and myofibroblasts, monocytes, neutrophils), inflammatory mediators (TNF-a, IL-6, IL-1b, CCL2, IL-8), and fibrotic mediators (TGF-β, collagen). This evidence concerns the gene IL1B and pulmonary fibrosis.