Since PD-L2 is substantially N-glycosylated at residues N64, N157, N163, and N189, the glycosylation of these sites except for N64 stabilizes PD-L2, reduces the killing ability of T-cells to cancer cells, and performs an essential function in mediating PD-1/PD-L2 interaction [56]. The gene discussed is PDCD1; the disease is cancer.