By deliveringmiRNA34a, we aimed to suppress the activity of PD-L1 surface markerson the cancer cells, thereby allowing T cells to gain strength andattack the cancer cells by various cytotoxic mechanisms.30 Initially, we had cocultured inactive JurkatT cells and A549 cells, subsequently stimulated Jurkat T cells totheir active states using anti-CD3/CD28, and cocultured active JurkatT cells with A549 cells. This evidence concerns the gene CD274 and cancer.