Our peptidomics platform confirmed higher oxidation of ApoB (one fragment) and ApoA‐I fragments (Table S9); intriguingly, in MASLD patients' sera compared to controls, we also found substantial MASLD‐associated changes in intact ApoC‐III glycoforms and fragments of ApoC‐III and ApoE, as well as a previously unreported increase in the oxidative state of these molecules. The gene discussed is APOE; the disease is metabolic dysfunction-associated steatotic liver disease.