In conclusion, our study reveals a novel mechanism by which SLAMF7 not only intrinsically enhances DNT antitumor function by regulating ERK-GPT2/SCL1A5-mediated glutamine metabolic pathway, but also engages in homotypic ligand-receptor interactions with SLAMF7-expressing tumor cells to promote DNT cell degranulation, thereby exerting a dual role in antitumor immunity. The gene discussed is GPT2; the disease is neoplasm.