The key to successful immune treatment is the establishment of long‐term protective immunity against cancer, but TCEs exert their antitumor function mainly by relying on TAA to redirect polyclonal T cells to kill target cells and are inefficient in inducing the formation of long‐lasting antitumor‐specific memory T cells.[31] Based on the data above, we hypothesized that PmTriTNE@CDA could redirect and expand CD8+ T cells while simultaneously reversing PD‐L1‐mediated immune suppression to kill tumor cells. The gene discussed is CD8A; the disease is neoplasm.