The overall efficacy for each formulation likely hinges on three rate limiting steps: (i) the tumor-intrinsic capacity to generate a sufficient range and scope of TAAs and TSAs presentable to both CD4+ and CD8+ T cells; (ii) the tumor-extrinsic aptitude for DCs to cross-present tumor antigens to prime sufficient anti-tumor T cell migration and effector responses leading to (iii) the total number of antigen-specific T cells capable of productive anti-tumor actions within the TME. The gene discussed is CD8A; the disease is neoplasm.