In turn, in the late phase of NAFLD, there was a prominent induction of LSECs’ pro-inflammatory phenotype characterized by increased PECAM-1, E-selectin, and ICAM-1 expression (Figure 2B–D) and significantly increased mRNA expression of COX-2, IL-6, NOX-2 (Figure 3B–D) and production of pro-inflammatory prostanoids such as PGE2 and PGF2a (Figure 4A,B). The gene discussed is ICAM1; the disease is metabolic dysfunction-associated steatotic liver disease.