Patients with fibrosing NASH may develop CVD events and undergo an acceleration of atherosclerosis, possibly via increased hepatic production of several prothrombogenic factors, such as vascular endothelial growth factor, hypoxia-inducible factor, intracellular adhesion molecule-1, vascular adhesion molecule-1, and fetuin-A [13]. The gene discussed is VEGFA; the disease is metabolic dysfunction-associated steatohepatitis.