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Figure 2. Natural killer (NK) cell antitumor immunity under histone deacetylase (HDAC) inhibitor influence. A tumor such as glioblastoma multiforme (GBM) is able to eschew immune surveillance by NK cells through either down regulation of surface marker [i.e., natural killer group 2D ligand (NKG2DL)] or through the activation of matrix metalloproteinases to degrade surface marker once they reach the tumor cell’s surface. Some selected HDAC inhibitors such as trichostatin A have been shown to upregulate surface markers in GBM. This upregulation of surface markers on the tumor cell’s surface makes the tumor able to be recognized by the immune system (through binding of natural killer group 2D to NKG2DL), causing the NK cells to release cytotoxic granules and leading to apoptosis in the GBM cell