On the one hand, NAFLD disease progression process can upregulate serum ferritin: one mechanism is that the excessive ferritin is released by damaged hepatocytes and/or systematic inflammation; inflammation can also upregulate hepcidin levels and result in dysmetabolic iron overload syndrome (DIOS), consequently raising up serum ferritin level; the p.C282Y homozygote HFE mutation in NAFLD patients is related to elevated transferrin saturation, accompanied by abnormally higher ferritin (13); further, signals that mediate NASH pathogenesis (e.g., TNF-α, IL-1β) can elevate ferritin level (33). This evidence concerns the gene IL1B and metabolic dysfunction-associated steatohepatitis.