In the pathogenesis of NASH, Povero et al. showed that free fatty acid-treated HepG2 cells release EVs enriched with the cell surface enzyme protein Vanin-1 (VNN1), and these EVs are efficiently taken up by human umbilical vascular endothelial cells (HUVEC) in a VNN1-dependent manner [101]. Here, VNN1 is linked to metabolic dysfunction-associated steatohepatitis.