Moreover, we also found that DON‐treated CD8 T cells showed upregulation of CD44 and CD62L and downregulation of exhaustion markers Lag3, PD‐1, and Tim3 (Figure 4D,E), which is consistent with previous results.[6] Considering the differential effects of glutamine antagonism to inhibit tumor cells while enhancing T cell function, we investigated the metabolic status of tumor cells, Th1 cells and CD8 T cells. Here, HAVCR2 is linked to neoplasm.