As it is revealed that SLC1A3 and GLUL are highly expressed in Macro_APOE/CTSZ while SLC1A5 and SLC38A1 are highly expressed in tumor cells in the current analysis, it may explain that excessive uptake of glutamine by tumor cells creates a shortage of glutamine in the TME, thereby triggering the acquisition of glutamate and synthesis of glutamine by TAM and further facilitating the immunosuppressive phenotype of TAM subpopulation. Here, SLC1A5 is linked to neoplasm.