Indeed, HDAC pharmacological inhibitors upregulate both MHC class I and II, together with CD40, CD80, and CD68 costimulatory molecules, as well as adhesion molecules such as ICAM-1 (Intercellular Adhesion Molecule 1) on tumor cells in the context of acute myeloid leukemia, neuroblastoma, hepatoma, and others, thus promoting natural killer cell-mediated lysis and CD8+ T cell response (148, 149, 159, 160). Here, CD8A is linked to neoplasm.