While many of the findings here mirrored previous findings of the important role of tumor-infiltrating CD8+ T cells, M1 macrophages, and T cell trafficking chemokines, this investigation demonstrated that the sustained pro-inflammatory response of entinostat and NHS-IL12 may be utilized for patients harboring innate and acquired resistance to checkpoint blockade therapies targeting the PD-1/PD-L1 axis. Here, CD274 is linked to neoplasm.