While studies have shown lower vascular endothelial growth factor A levels in NASH patients compared to healthy controls or to patients with bland steatosis, hepatic angiogenesis driven by vascular endothelial growth factor A is thought to aid fibrogenesis; therefore, possible interventions targeting LSEC-mediated HSC inactivation should concentrate on downstream effectors [134,135,136]. This evidence concerns the gene VEGFA and steatosis.