In PAH, sST2 has been proposed as a prognostic biomarker with elevated levels correlating with right ventricular dysfunction and increased mortality risk.25 Elevated circulating sST2 levels may originate from myocardial stress, as well as from vascular remodeling in the pulmonary arteries.26 High sST2 levels might also reflect a compensatory mechanism to counteract the detrimental effects of elevated IL-33 in the lungs. Here, IL33 is linked to pulmonary arterial hypertension.