Disrupted nitric oxide (NO) synthesis is a hallmark of PH pathophysiology.10 The primary receptor for NO is soluble guanylyl cyclase (sGC), which, upon activation by NO, catalyzes the formation of cyclic guanosine monophosphate from guanosine triphosphate,11,12 promoting vasodilation and smooth-muscle relaxation.13 Studies show that both NO and cyclic guanosine monophosphate production decrease in models of cirrhosis, leading to HSC activation.14,15 Activated HSCs constrict hepatic sinusoids by adopting contractile characteristics causing restricted portal flow, promoting venous congestion. Here, SGCB is linked to Cirrhosis.