SLC38A1 and neoplasm: 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.