Previous animal studies involving bleomycin-induced pulmonary fibrosis mouse models showed that the absence or inhibition of PAR2 was associated with a significant reduction in various pro-fibrotic measurements, including a reduction in total lung collagen, reduction in epithelial-mesenchymal transition, reduction in severity and extent of fibrotic lesions, and reduction in pro-fibrotic signaling molecules such as TGF-β and monocyte chemotactic protein 1 (MCP-1), also known as CCL2 [22, 45, 46]. Here, TGFB1 is linked to pulmonary fibrosis.