Following binding and specific recognition, effector T cells are ultimately activated through signaling pathways such as mitogen-activated protein kinase (MAPK), leading to the destruction of tumor cells [12].However, within the tumor microenvironment, when PD-1 on T cells interacts with PD-L1 on tumor cells or APCs, the immunoreceptor tyrosine-based inhibitory motifs (ITIMs) and immunoreceptor tyrosine-based switch motifs (ITSMs) of PD-1 become phosphorylated.This process recruits and activates SHP-2, which effectively inhibits T cell activation. This evidence concerns the gene CD274 and neoplasm.