To identify the pathological molecular mechanisms induced by KCNK3 loss of expression in hPASMCs and hPAECs, we postulated that a differential proteomic analysis between siControl and siKCNK3 conditions would identify the crucial signaling pathways to better understand the contribution of KCNK3 dysfunction to PAH pathobiology. The gene discussed is KCNK3; the disease is pulmonary arterial hypertension.