By extension, as KCNK9 and KCNK3 are co-expressed in a variety of tissues outside the lungs, it was proposed that perhaps the absence of KCNK9 in the lungs may underlie the lung-specific phenotype observed in PAH patients due to KCNK3 mutation, and KCNK9 gene therapy may represent a novel therapeutic approach to PAH due to KCNK3 dysfunction [21]. This evidence concerns the gene KCNK9 and pulmonary arterial hypertension.