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It is presumed that cysteine can bind to copper at the active site of the TYR, inactivating the enzyme, and the substrates block cysteine’s access to the active site of the enzyme

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Tumor‐Associated Macrophages Ginsenoside Rb1 promotes macrophage polarization toward the M1 phenotype with antitumor functions by regulating the NF‐κB signaling pathway, while simultaneously enhancing phagocytic activity [225]