In the context of cancers, PD-L1 binding to PD-1 on tumor-specific cytotoxic T lymphocytes (CTLs) can recruit SHP2 to the C-terminal of the PD-1 intracellular domain, leading, subsequently, to the inhibition of downstream PI3K/Akt signaling, which would downregulate cell survival gene BCL-XL expression and result in the dysfunction or apoptosis of T cells [21,34,35,36]. This evidence concerns the gene CD274 and neoplasm.