Deletion of Id2 suppresses CD8+ T cell-mediated immune responses and the persistence of stem-like CD8+ T cell subsets, consequently compromising the effectiveness of PD-1 blockade and increasing susceptibility to tumor development.101 The maturation of CD8+ T cells is modulated by various transcriptional regulators, including NFAT, NR4A, and TOX.102 Conversely, in a melanoma mouse model, transcription factors BATF and IRF4 impede T cell differentiation.103 Essentially, the goal of ICB therapy is to alleviate immune exhaustion and T cell decline in anti-cancer efforts. Here, CD8A is linked to neoplasm.