CD8+ TEXs suffered from severe suppression of glycolysis and oxidative phosphorylation (OXPHOS) and increased lipid peroxidation and endoplasmic reticulum (ER) stress, which damaged the effector function of tumor infiltrating CD8+ T cells (CD8+ TILs) and promoted terminal exhaustion differentiation (Figure 2) (3, 36, 37). Here, CD8A is linked to neoplasm.