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Mechanistic studies reveal that SFN significantly downregulates programmed death-ligand 1 (PD-L1) expression on tumor cells through multiple mechanisms, including direct covalent modification of cysteine residues on STAT1, which inhibits its transcriptional activity and blocks IFN--induced PD-L1 expression ( The immunomodulatory effects of SFN extend to comprehensive reprogramming of immune cell populations within the tumor niche

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The malate can then be decarboxylated to pyruvate via mitochondrial malic enzyme