Dendritic cells (DCs) are pivotal drivers of anti-tumor immunity, but many of the DCs in tumors appear dysfunctional or immunosuppressive. Using mouse models, we found that robustly immunogenic DCs can arise by differentiation from immature myeloid precursor cells during inflammation. In tumors, however, differentiation of these inflammatory DCs was blocked by a cell-intrinsic signaling pathway created by Bruton’s Tyrosine Kinase (BTK) and the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase (IDO). Overall design: The immature (CD11cNEG Ly6c+c-kit+) cells were sorted from TDLNs of untreated B16F10 tumors, and analyzed by RNA-seq. Three identical replicate experiments were performed (labeled .1, .2, .3). Results were compared against analysis of publically-available datasets for conventional cDC1 cells.