EVs from portal myofibroblasts were proposed to function in hepatic vascular remodeling and the production of scar tissue because progression to cirrhosis involved the production of collagen 15A1-positive portal myofibroblasts, which localized to vessels in fibrotic septa and released vascular endothelial growth factor A (VEGFA)-rich microparticles that stimulate VEGF receptor 2 activation and tube formation in endothelial cells [268]. This evidence concerns the gene VEGFA and Cirrhosis.