TGFB1 and pulmonary fibrosis: Next, we investigated whether butaprost mitigated the pro‐fibrotic effects of TGF‐β via the cAMP pathway, which has been shown to play a role in pulmonary fibrosis.10 It has been demonstrated that activation of the EP2 receptor increases intracellular cAMP levels.3 Indeed, treatment with butaprost markedly increased intracellular cAMP levels; however, this response was suppressed in presence of TGF‐β (Figure 2A).