In addition, TAMs and TME mediators (e.g., exosomal PD-L1 and VEGF) inhibit the extravasation of CD8+ T cells from the circulatory system, as well as the replication and viability of CD8+ T cells within a tumour.79 In models of colorectal cancer and mesothelioma, the depletion of TAMs restored CD8+ cell infiltration and migration within tumours and improved the efficacy of anti-PD-1 immunotherapies.79 The gene discussed is PDCD1; the disease is neoplasm.