This prolonged activation can promote the production of inflammatory cytokines, such as IL-6 and IL-4, and tumor metabolism-related factors, such as indoleamine-2,3-dioxygenase, facilitating the formation of the tumor microenvironment (TME) and attenuating the effects of immune checkpoint blockade therapies, including PD-1 (programmed cell death protein 1)/PD-L1 (programmed cell death ligand 1) inhibitors. This evidence concerns the gene PDCD1 and neoplasm.