Their dual activity in cross-priming anti-tumor CTL within lymph nodes and restimulating CTL within tumors probably contributes to the general Batf3-dependence of anti-tumor immunity that has been observed in mice (Diamond et al., 2011; Fuertes et al., 2011; Hildner et al., 2008) and to the suppression of anti-tumor immunity by PGE2 that we observe here. The gene discussed is BATF3; the disease is neoplasm.