During NASH progression, LSECs acquire a pro-inflammatory phenotype characterized by overexpression of adhesion molecules at their surface, including intracellular adhesion molecule 1, vascular cell adhesion molecule 1, and vascular adhesion protein 1, as observed in mouse models of NASH and patients, contributing to leucocyte recruitment into the liver [112,113]. Here, VCAM1 is linked to metabolic dysfunction-associated steatohepatitis.