In MASH patients, liver angiogenesis supports fibrosis through mechanisms like tissue hypoxia, hepatocyte-derived microvesicles, angiopoietin-2 expression, and elevated leptin levels with a direct pro-fibrotic effect by upregulating TGF-β in LSECs and KCs [7]. The gene discussed is LEP; the disease is metabolic dysfunction-associated steatohepatitis.