Intriguingly, also the oxidation of ApoE fragment was increased in MASLD; this could contribute to the loss of function of this apolipoprotein and delay the hepatic uptake (catabolism) of ApoB containing lipoproteins, thus potentially further promoting the hypertriglyceridemic state often observed in MASLD patients [62]. This evidence concerns the gene APOB and metabolic dysfunction-associated steatotic liver disease.