We solved this issue via co‐delivering epigenetic bromodomain inhibitor OTX which suppresses the expression of PD‐L1 and generates robust anti‐tumor responses, turning the “cold” immunosuppressive GBM into T cell inflamed “hot” tumors with significant increased dendritic cells (CD80, CD86), anti‐tumor T cells (CD4+, CD8+), and results in the second synergetic inhibition effect for GBM treatment (Figure 2A): 3) OTX itself can also induce GBM cell apoptosis via inducing cell cycle arrest which improves the GBM therapy of TMZ. The gene discussed is CD86; the disease is neoplasm.