Indeed, many of the cardio- and vasoprotective actions of endogenous CNP, including antiproliferative effects on smooth muscle cells, vasorelaxation, inhibition of leukocyte recruitment, and antifibrotic capacity (10, 11), might be anticipated to counteract the key drivers of MASH and cirrhosis, including portal hypertension, hepatic inflammation, HSC proliferation, and hepatic fibrosis; indeed, there is increasing recognition that MASH is a vascular disease of the liver (14). The gene discussed is CNP; the disease is portal hypertension.