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Abstract Glutamine (Gln) metabolism serves dual metabolic roles: it fuels the tricarboxylic acid (TCA) cycle, while concurrently sustaining redox balance through glutathione (GSH) synthesis

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RBM4 dictates ESCC cell fate switch from cellular senescence to glutamine-addiction survival through inhibiting LKB1-AMPK-axis

However, the mechanism of action of glutamine in the immune cells of cancer patients remains unclear, and further research is needed on the inhibitors of glutamine metabolism and their mechanisms of action, as well as the potential broader application of combined immune checkpoint inhibitors