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Additionally, the interaction between co-inhibitory and co-stimulatory pathways (e.g., TIGIT/CD226) is complex and not entirely understood, complicating the development of medicines that optimize efficacy without inducing undesirable immune activation (73, 81)

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This role is best illustrated in glutamine’s importance to the TCA cycle and specifically to α-KG levels, as this metabolite can act as a co-activator of Jumonji-C domain containing histone demethylases and TET demethylases