PD-L1+ T cells exerted tumour-promoting tolerance [232] via (1) binding of PD-L1 induced STAT3 (signal transducer and activator of transcription protein 3) -dependent ‘back-signalling’ in CD4+ T-cells, which prevented activation [233]; (2) PD-L1+ T-cells restraining effector T-cells and accelerating tumorigenesis, even in the absence of endogenous PD-L1 and (3) PD-L1+ T-cells engaging PD-1+ macrophages [234], inducing an alternative M2-like program, which had crippling effects on adaptive antitumor immunity. Here, CD4 is linked to neoplasm.