These observations provide a hint that repressive epigenetic modifications at the COX-2 promoter could be introduced, at least to some extent, by TGFβ1 treatment and that endogenously produced PGE2 after COX-2 reexpression could play a key role in preventing and reversing lung fibroblast activation in IPF. This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.