Belinostat, a potent pan HDAC inhibitor, causes H3 subunit acetylation and induces HTLV-1 Tax expression in cultured ATLL cells resulting in dose-dependent apoptosis. Further, Belinostat blocks constitutive expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and increases apoptosis in the presence of AZT.