Specific ablation of PD-1 on intratumoral DCs resulted in enhanced priming of tumor-specific CD8 T cells, which exhibited increased expression of the cytolytic molecules perforin and granzyme-B.39 Additionally, PD-1 inhibition increases DC expression of the costimulatory molecules, CD40, CD80, and CD86,43 which may be due to increased MAPK signaling.41 The above studies demonstrate that PD-1 regulates DC function both directly and indirectly within the inflammatory TME. The gene discussed is CD8A; the disease is neoplasm.