We have previously reported that fibroblasts derived from the lungs of patients with IPF and SSc exhibit reduced capacity to up-regulate cyclooxygenase-2 (COX-2, PTGS2) and its downstream anti-fibrotic product prostaglandin (PG) E2, compared with control lung fibroblasts, and that this imparts a functionally profibrotic phenotype to the cells [6]. This evidence concerns the gene PTGS2 and idiopathic pulmonary fibrosis.