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Furthermore, enhanced glutamine metabolism has been shown to significantly increase -KG production, which, in turn, activates the mTOR1 signaling pathway and further inhibits the autophagy-promoting kinase (APCK) of the ULK1 complex by mediating site-specific phosphorylation of ULK1 (Ser637 and Ser757) and Atg13 (Ser258) activity, thereby promoting cancer cell proliferation [27]