During NASH, inflammation and gut microbiota-derived signals could increase the NF-kB pathway activation in LSECs, which coordinate the release of pro-inflammatory mediators including MCP1, IL1, IL6, TNFα, and the upregulation of adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion protein-1 (VAP-1). Here, CCL2 is linked to metabolic dysfunction-associated steatohepatitis.