In preclinical studies, HDAC inhibitors (HDACi) have proven to be effective anti-GB agents via multiple mechanisms, such as upregulating the expression of tumor suppressor genes, inhibiting oncogenes, inducing cell cycle arrest, promoting cell apoptosis and differentiation, inhibiting motility/migration, abolishing autophagy and tumor angiogenesis, and upregulating natural killer (NK)-cell-mediated tumor immunity [212,213,214,215]. Here, HDAC9 is linked to neoplasm.