Using an oncogenic K-ras-driven PDAC mouse model (KPC mice), we found that signaling via TNFR1, but not TNFR2, in cells of the immune system profoundly limits tumor-infiltrating DC number and function, and its abrogation by genetic or therapeutic means led to a marked increase in DC infiltration and activation, and a more effective anti-tumor response. The gene discussed is TNFRSF1A; the disease is neoplasm.