suggested that glutamine metabolism could support highly immunosuppressive tumor-infiltrating immature myeloid cells with glutamine-derived α-ketoglutarate, and could also regulate their suppressive capacity through the glutamate-NMDA receptor axis, in which inhibiting GLS1 improved the efficacy of anti-PD-L1 treatment, with decreased Arginase1+ myeloid cells, increased CD8+, IFNγ+, as well as granzyme B+ T cells, and delayed tumor growth in an immunotherapy-resistant mouse model (104). Here, CD8A is linked to neoplasm.