As MASLD progresses, LSECs acquire a pro-inflammatory phenotype, overexpressing adhesion molecules such as ICAM-1, VCAM-1, E-selectin, and VAP-1 at the surface of LSECs and producing inflammatory mediators, including TNFα, IL-6 and IL-1 [52]. This evidence concerns the gene IL6 and metabolic dysfunction-associated steatotic liver disease.