As cirrhosis progresses, hyperdynamic circulation cannot compensate for the splanchnic vasodilation and results in the activation of the renin–angiotensin–aldosterone system (RAAS), sympathetic nervous system (SNS), and at later stages, inducing non-osmotic secretion of arginine–vasopressin (AVP) to maintain increased effective arteriolar volume. This evidence concerns the gene AVP and Cirrhosis.