In the absence of KCNK3 mutations, we found a reduced TASK-1 function or expression in lung or isolated pulmonary arteries (PA) from heritable PAH (BMPR2 carriers patients) and iPAH patients, as well as in isolated PASMCs, demonstrating that reduced KCNK3 function/expression is a hallmark of PAH at the pulmonary vascular level [7]. Here, KCNK3 is linked to pulmonary arterial hypertension.