Programmed cell death protein 1 (PD-1) plays an important role in subsiding immune responses and promoting self-tolerance through suppressing the activity of T cells and promoting differentiation of regulatory T cells. PD-1 is considered as an immune checkpoint and protects against autoimmune responses through both induction of apoptosis in antigen-specific T cells and inhibiting apoptosis in regulatory T cells. After PD-1 binding to its ligands, the active immune cells are inhibited. Two known ligands of PD-1 are PD-L1 and PD-L2, which belong to the B7 family. Accumulative evidence has established that the blockade of the inhibitory effects of PD-1 can elicit effective immune responses against tumor cells. PD-1 signaling pathway blockade has shown clinical responses in patients with different solid tumors and hematological malignancies[1].