This intense dTeff infiltration is in fact initiated and maintained by higher levels of DCm (Fig. 5).These results provide a mechanistic rationale underlying variability in CT26 tumor growth dynamics and in their responses to RT and anti-PD-L1 treatments, and demonstrate that an early onset and effective nTeff infiltration, supported by higher and sufficiently sustained levels of DCm, are necessary to overcome the development of immuno-suppression within the TME and to ultimately achieve tumor rejection. The gene discussed is CD274; the disease is neoplasm.