Regarding the involvement of Kcnk3 dysfunction in the proliferative phenotype of PAH PASMC, we found that the knockdown of KCNK3 in control hPASMCs enhances hPASMC proliferation in correlation with an increase of HIF-1α expression and over-phosphorylation of ERK1/2, which are hallmarks of proliferation/apoptosis imbalance and PAH development. This evidence concerns the gene MAPK3 and pulmonary arterial hypertension.