Emerging studies suggest that tumor-cell-intrinsic factors contribute to the level of immune infiltration into the tumors and the tumor immune escape. Therefore, it is critical to understand the relationship between tumor-cell-intrinsic factors and the immune response. High-mobility group box protein 1 (HMGB1) is a protein with diverse roles both in the intracellular and extracellular environments. In cancer, HMGB1 manifests both protumoral and antitumoral properties. Yet, it is not clear if the tumor-cell-intrinsic roles of HMGB1 influence immune cell infiltration in tumors. In this thesis, we demonstrated that downregulation of HMGB1 in cancer cells reduced the tumor growth in mice and led to a local reprogramming of the tumor microenvironment. The reduction of tumor growth was T-cell mediated, due to activation of both afferent and efferent pathways resulting in elevated numbers of intratumoral T-cells through enhanced infiltration, highlighting the importance of tumor-cell-intrinsic HMGB1 in immunosurveillance and immune evasion.