In addition to promoting effector CD8+ T cell differentiation against established tumors with IL‐12 or BMDC vaccination as we have previously reported [14, 17], it might also be possible to drive complete effector differentiation of sub‐optimally stimulated T cells by enhancing the immunogenicity of endogenous cross‐presenting DC, either with interventions that promote immunogenic tumor cell death or by using approaches to expand and activate these cells in situ [29]. The gene discussed is CD8A; the disease is neoplasm.