Low levels of chronic inflammation and lipid accumulation in the liver are considered the core pathogenic underpinnings of NAFLD [11]; the resulting lipid metabolism disorder, IR, and enteric endotoxin contribute to the production and release of proinflammatory factors tumor necrosis factor (TNF)-α, interleukin- (IL-) 1B, and IL-6 [12]. This evidence concerns the gene IL6 and metabolic dysfunction-associated steatotic liver disease.