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The downstream substrates of mTORC1, such as 4EBPs, S6K1, and unc-51-like kinase 1 (ULK1), are markers for detecting mTORC1 activity (51)

These data point to a previously unrecognized effect of KG-mediated epigenetic rewiring through histone acetylation

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By conducting in-depth analysis of the diet-microbiota-immunometabolism regulatory network, through targeted dietary modifications to adjust nutrient availability in the TME, reshaping the gut microbiota with probiotics or prebiotics to enhance immunometabolic activity, and combining immune checkpoint inhibitors with metabolism-targeted drugs, it may be possible to disrupt tumor metabolic adaptation and immune escape at a systemic level, thereby achieving personalized and precision therapy