In the bleomycin-induced rat model of IPF, aberrant expression of STAT1, excessive platelet-derived growth factor (PDGF) secretion, and increased plasminogen activator inhibitor-1 (PAI-1) expression positively correlate with collagen content, suggesting the potential involvement of the JAKs/STATs signaling pathway in the IPF process [50]. The gene discussed is SERPINE1; the disease is idiopathic pulmonary fibrosis.