Collectively, this study demonstrated that ACM derived from both early and late-stage OGJ patients upregulates inhibitory ICs TIGIT, A2aR, PD-L2 and CD160 on the surface of T cells and specifically upregulates CTLA-4 on the surface of Th1-like cells and Treg cells thus, creating a therapeutic vulnerability that may be exploited by ICBs to harness anti-tumour immunity. The gene discussed is PDCD1LG2; the disease is neoplasm.