Subsequently, the soluble guanylate cyclase (sGC) in the vascular smooth muscle cells could be activated, converting guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP), thereby activating cGMP-dependent protein kinases G (PKG), leading to vasodilation and limiting pulmonary hypertension [20–22]. The gene discussed is PRKG1; the disease is pulmonary arterial hypertension.