PDCD1 and neoplasm: Not only checkpoint inhibitor therapies promote the direct anti-tumor efficacy of NK cells, but also, NK cells can promote stimulatory DCs recruitment to tumor sites by secreting cytokine Fms-related tyrosine kinase 3 ligand (FLT3LG), which subsequently enhances the responses of patients to anti-PD-1 therapy and promotes increased overall survival (148, 149).