Chronic activation of T cells in the tumor microenvironment (TME) results in upregulation of an inhibitory receptor, programmed cell death protein 1 (PD-1), which interacts with programmed death-ligand 1 (PD-L1) on tumor cells and/or bystander cells for functional suppression and exhaustion [3,4]. The gene discussed is PDCD1; the disease is neoplasm.