Commensurately, dramatically reduced numbers of CD103+CD11c+ DCs in tumor from DEXP&A&N-treated Batf3−/− mice (Additional file 1: Figure S5c and S5d) resulted in greatly decreased tumor-infiltrating CD8+ T cells (Fig. 5f) and tumor retardation (Additional file 1: Figure S5e), compared to wild-type mice, demonstrating that host Batf3-dependent cross-presenting DCs and T cells are primarily responsible for the antitumor immunity of DEXP&A&N. Here, BATF3 is linked to neoplasm.