In pediatric populations particularly, this leads to hepatic steatosis that establishes a self-perpetuating metabolic cycle characterized by two interconnected pathological processes: (1) disrupted lipid homeostasis due to impaired regulation of free fatty acid flux, hepatic triglyceride synthesis, and clearance pathways (β-oxidation and VLDL secretion) [12, 31] and (2) chronic low-grade inflammation driven by elevated proinflammatory cytokines (IL-6, TNF-α, CRP) coupled with reduced adiponectin production [35]. This evidence concerns the gene IL6 and fatty liver disease.