Based on the fact that conditional ablation of PD-L1 in T-cells promoted adaptive anti-tumor responses and activated macrophages, they elucidated that PD-L1+ T-cells reinforce an immune tolerant environment to accelerate carcinogenesis through three ways: (1) PD-L1 engagement on T-cells inhibits Th1 differentiation but promotes Th17 differentiation via a STAT3-dependent manner, while inducing an anergic phenotype in CD8+ T-cells (2) PD-L1+ T-cells deliver inhibitory signals to PD-1+ T-cells; (3) PD-L1+ T-cells engage PD-1+ macrophages to promote M2-preference differentiation. The gene discussed is PDCD1; the disease is neoplasm.