The article reviews the role of histone deacetylases (HDACs) in human cancer. HDACs are enzymes that catalyze the removal of acetyl groups from histone proteins, which can lead to gene silencing. Altered expression and mutations of HDACs have been linked to tumor development by inducing aberrant transcription of key genes involved in cell proliferation, cell cycle regulation, and apoptosis. The balance of histone acetylation and deacetylation is crucial for chromatin remodeling and gene transcription. HDACs can also regulate gene expression by forming corepressor complexes with nuclear receptors and interacting with transcription factors. In cancer, the loss of acetylated histone modifications and hyperacetylation of histone H4 are common events, often occurring early in tumorigenesis. Overexpression of HDACs in various cancers has been observed, and their recruitment to specific promoters through interactions with fusion proteins is a significant mechanism in hematological malignancies. SIRT1, a class III HDAC, plays a role in regulating gene expression, apoptosis, and DNA repair, and its deregulation is associated with cancer development. HDAC inhibitors have shown promise as anticancer agents, and clinical trials are ongoing to evaluate their efficacy in treating hematological and solid tumors.The article reviews the role of histone deacetylases (HDACs) in human cancer. HDACs are enzymes that catalyze the removal of acetyl groups from histone proteins, which can lead to gene silencing. Altered expression and mutations of HDACs have been linked to tumor development by inducing aberrant transcription of key genes involved in cell proliferation, cell cycle regulation, and apoptosis. The balance of histone acetylation and deacetylation is crucial for chromatin remodeling and gene transcription. HDACs can also regulate gene expression by forming corepressor complexes with nuclear receptors and interacting with transcription factors. In cancer, the loss of acetylated histone modifications and hyperacetylation of histone H4 are common events, often occurring early in tumorigenesis. Overexpression of HDACs in various cancers has been observed, and their recruitment to specific promoters through interactions with fusion proteins is a significant mechanism in hematological malignancies. SIRT1, a class III HDAC, plays a role in regulating gene expression, apoptosis, and DNA repair, and its deregulation is associated with cancer development. HDAC inhibitors have shown promise as anticancer agents, and clinical trials are ongoing to evaluate their efficacy in treating hematological and solid tumors.