PD-1 and its ligands, PD-L1 and PD-L2 expressed within the tumor microenviroment, can modulate the balance between T-cell activation, tolerance, and immunopathology during long-term antigen exposure.[70,71] To evade from the immune system's monitoring, tumor cells in tumor microenvironment can upregulate the expression of PD-L1 through a variety of mechanisms, and bind themselves with negative immune checkpoint PD-1 on the surface of T cells, thereby inhibiting T cells function, losing its killing effect on tumor cells.[71]. This evidence concerns the gene CD274 and neoplasm.