It is conceivable that in NASH HCCs overexpression of enzymes involved in energy metabolism, extracellular matrix proteins, vimentin, actin cytoskeleton members, and those involved in DNA repair of double strand breaks and oxidative base modifications, is likely to be mediated by TGF-β, β-catenin, Nrf2, SP1, EGFR, PDGF, FGF2, VEGFA, IL1A, IL1B and other factors, which may explain lowered apoptosis and increased survival, migration and invasion activity of NASH liver cells. Here, IL1A is linked to metabolic dysfunction-associated steatohepatitis.