This reduction in COX-2 expression in fibroblasts from IPF lungs was attributed to the inability of transcriptional factors such as NF-κB/p65, CEBPb, and CREB-1 to bind to COX-2 promoter due to a defective H3 and H4 histone acetylation resulting from increased recruitment of HDACs and decreased HATs [54]. Here, PTGER2 is linked to idiopathic pulmonary fibrosis.