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revealed that CDKN2A deletion reshaped the lipidome of GBM, redistributing oxidative PUFAs to distinct lipid compartments, thereby increasing lipid peroxidation levels and significantly increasing sensitivity to ferroptosis ( in vivo ( 2.3 Imbalance of the antioxidant defense system The occurrence of ferroptosis in GBM cells not only depends on the activation of death signaling but is also closely related to the functional imbalance of the endogenous antioxidant defense system

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Individuals with PNPLA3 I148M variants, associated with non-alcoholic fatty liver disease, demonstrate differential methylation responses to dietary choline and fermented foods, suggesting that epigenetic regulation may mediate genediet effects on liver health [15,16]

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