Across the three representative systems, all platforms converged on inducing immunogenic cell death (ICD) and promoting CD4+/CD8+ T-cell infiltration, yet each pursued distinct design logics: gemcitabine–PheoA liposomes prioritized drug stability and dual chemo–PDT action, ER-biomimetic liposomes leveraged organelle selectivity to amplify ER stress-driven ICD and checkpoint blockade synergy, and polymer-reinforced antigen-capturing liposomes established durable immune memory by stabilizing vesicle architecture and retaining tumor-associated antigens. This evidence concerns the gene CD8A and neoplasm.