HDAC9 and neoplasm: TSA, a hydroxamic acid-based HDAC inhibitor, chelates zinc in the HDAC active site and stabilizes binding through hydrophobic interactions. This inhibition leads to chromatin relaxation and reactivation of silenced genes, sensitizing tumor cells to OV infection. In combination with oHSV, TSA enhances antitumoral and antiangiogenic effects, promotes viral replication, and improves therapeutic efficacy.