Determining the mechanism of NK cell recruitment could potentially lead to direct targeting of NK cell recruitment as a therapeutic target to start the tumor-immune “relay race.” This therapeutic approach could convert immunotherapy-resistant, non-T cell-inflamed tumors into checkpoint blockade therapy-sensitive T cell-inflamed microenvironments, potentially independent of the tumor type and molecular mechanism for exclusion of CD103+ DC and CD8+ T cells. This evidence concerns the gene CD8A and neoplasm.