In conclusion, our findings that CSE induced an imbalanced prostanoid release characterised by the reduced PGI2/TXA2 ratio, likely as a result of an imbalanced expression of PGIS and TXAS, and that agents targeting the imbalance inhibited CSE-induced pulmonary artery cell proliferation point to TXA2 as a novel mediator of pulmonary artery cell dysfunction and proliferation in pulmonary hypertension in COPD and strongly suggest that targeting the imbalance may have therapeutic potentials for this fatal disease and that smoking cessation may prevent further vascular remodelling. This evidence concerns the gene TBXAS1 and pulmonary arterial hypertension.