Particularly, PD-1 blockade under suboptimal priming conditions leads to the emergence of a subset of dysfunctional CD8+ T cells that prevent antitumor immunity.225 However, these observations have catalyzed exploration into novel co-inhibitory molecules expressed on exhausted T cells with the goal of identifying receptors with more tumor-restricted expression to achieve increased efficacy while limiting autoimmune-like toxicity. The gene discussed is PDCD1; the disease is neoplasm.