Histone deacetylase (HDAC) inhibitors are promising anticancer drugs that target epigenetic processes, influencing gene expression through acetylation of histones and other proteins. These inhibitors induce cancer cell cycle arrest, differentiation, apoptosis, and reduce angiogenesis and immune response modulation. They act through various mechanisms, including cell cycle arrest, apoptosis induction, autophagy, and effects on non-coding RNA and signaling pathways. HDAC inhibitors can be classified into different types, such as hydroxamic acids, short-chain fatty acids, benzamides, cyclic tetrapeptides, and sirtuin inhibitors. Approved HDAC inhibitors include vorinostat, romidepsin, belinostat, and panobinostat, which are used for treating T-cell lymphomas and multiple myeloma. Other HDAC inhibitors are under clinical trials for various cancers. HDAC inhibitors show synergistic effects when combined with other anticancer therapies, such as chemotherapy, radiotherapy, and DNA-damaging agents. Clinical studies indicate that HDAC inhibitors can enhance the efficacy of existing treatments and improve patient outcomes. However, further research is needed to optimize their use, understand their mechanisms, and determine the most effective combinations for different cancer types. The reversibility of epigenetic changes makes HDAC inhibitors a promising therapeutic approach.Histone deacetylase (HDAC) inhibitors are promising anticancer drugs that target epigenetic processes, influencing gene expression through acetylation of histones and other proteins. These inhibitors induce cancer cell cycle arrest, differentiation, apoptosis, and reduce angiogenesis and immune response modulation. They act through various mechanisms, including cell cycle arrest, apoptosis induction, autophagy, and effects on non-coding RNA and signaling pathways. HDAC inhibitors can be classified into different types, such as hydroxamic acids, short-chain fatty acids, benzamides, cyclic tetrapeptides, and sirtuin inhibitors. Approved HDAC inhibitors include vorinostat, romidepsin, belinostat, and panobinostat, which are used for treating T-cell lymphomas and multiple myeloma. Other HDAC inhibitors are under clinical trials for various cancers. HDAC inhibitors show synergistic effects when combined with other anticancer therapies, such as chemotherapy, radiotherapy, and DNA-damaging agents. Clinical studies indicate that HDAC inhibitors can enhance the efficacy of existing treatments and improve patient outcomes. However, further research is needed to optimize their use, understand their mechanisms, and determine the most effective combinations for different cancer types. The reversibility of epigenetic changes makes HDAC inhibitors a promising therapeutic approach.