Under normal circumstances, circulating levels of serotoninare low, as excess could promote harmful inflammation, proliferationand vasoconstriction in the pulmonary circulation.24 Disruption of serotonin homeostasis by selective serotoninreceptor uptake inhibitors was associated with increased clinicalworsening events and mortality in PAH.25 Furthermore, increased SERT activity has been observed in PASMC.26 Interestingly, defective platelet serotonin storage can persistdespite ‘curative’ heart–lung transplantation.27 This evidence concerns the gene SLC6A4 and pulmonary arterial hypertension.