Another major mechanism for progressing tumors to evade ICD at the execution phase (ie, the ability of ICD-driven CTLs to mediate cytotoxic effects) relies on immune exhaustion, that is, the establishment of dysfunction in tumor-infiltrating T cells.238–241 Coinhibitory receptors including programmed cell death 1 (PDCD1, also known as PD-1) are major (but not the sole) players in this setting. This evidence concerns the gene PDCD1 and neoplasm.