Although the mechanistic contributions of intestinal immune dyshomeostasis to NAFLD pathogenesis require further elucidation, consistent evidence from human studies and animal models demonstrates immune cell infiltration indicative of mucosal inflammation and elevated pro-inflammatory cytokine profiles (e.g., TNF-α, IL-6, IL-1β) during both NAFLD and NASH progression [81, 82]. The gene discussed is TNF; the disease is metabolic dysfunction-associated steatotic liver disease.