Intriguingly, long-lasting contacts between macrophages and CD8+ T cells in surgically resected NSCLC tumors are associated with impaired motility and reduced infiltration of lymphocytes in tumor islets; in pre-clinical models resistant to anti-PD-1, the concomitant depletion of macrophages can restore T cell motility and infiltration into tumor islets with increased tumor cell killing, suggesting that myeloid cells can modulate the TME not only through soluble mediators but also by physical contact with the surrounding cells (86). This evidence concerns the gene PDCD1 and neoplasm.