Firstly, SLAMF7 could upregulate GPT2/SLC1A5-mediated glutamine metabolism by activating ERK signaling pathway in DNT, thereby supporting mitochondrial fitness, increasing ATP production, enhancing the expression of effector molecules such as granzyme B and perforin, and promoting antitumor activity of DNT against tumor cells independent of homotypic ligand-receptor interactions. The gene discussed is GPT2; the disease is neoplasm.