SOCS3 and metabolic dysfunction-associated steatotic liver disease: TNFα, IL6, IL1β, CXCL8 and TGFβ, which are obvious actors in the pathogenesis of progressive NAFLD, are involved in hepatocytes death/apoptosis (TNFα, TGFβ), neutrophil chemotaxis (CXCL8), activation of hepatic cells (TNFα, TGFβ), Mallory-Denk bodies (TNFα, TGFβ) and hepatic insulin resistance (TNFα, IL6, IL1β and SOCS3) [25].