The article "Epigenetic Cancer Therapy" by Nabanita Das and Tapas K. Kundu discusses the role of epigenetics in cancer and the potential of epigenetic therapies. Epigenetics involves the regulation of gene expression through modifications of DNA, histone proteins, and small non-coding RNAs. These modifications are reversible and influenced by the cell's metabolic state. Enzymes like DNA methyltransferases (DNMTs), lysine acetyltransferases (KATs), and lysine methyltransferases (KMTs) are responsible for these modifications, while "erasers" remove them to maintain cellular homeostasis. Cancer is often characterized by dysregulated epigenetic machinery, making these enzymes and their inhibitors promising targets for cancer treatment. Historically, chemotherapeutics have targeted the epigenome, with nucleotide analogues being widely used. Recent studies have identified overexpression of DNMTs, histone deacetylases (HDACs), and other epigenetic enzymes in cancer cells. Hyperactivity of these enzymes is linked to various types of cancer, and their inhibition can enhance the effectiveness of chemotherapeutics. For example, the epigenetic silencing of SALL2 confers tamoxifen resistance in breast cancer, which can be overcome by inhibiting the histone methyltransferase EZH2. The article highlights the development of inhibitors for DNA methyltransferases, HDACs, and other epigenetic enzymes, many of which are already approved or in advanced clinical trials. Natural compounds are also being explored for their potential to modulate epigenetic enzymes, either alone or in combination with chemotherapeutics to reduce toxicity. Additionally, epigenetic modifications may serve as diagnostic markers for cancer progression and prognosis. The authors acknowledge support from various institutions and declare no conflict of interest.The article "Epigenetic Cancer Therapy" by Nabanita Das and Tapas K. Kundu discusses the role of epigenetics in cancer and the potential of epigenetic therapies. Epigenetics involves the regulation of gene expression through modifications of DNA, histone proteins, and small non-coding RNAs. These modifications are reversible and influenced by the cell's metabolic state. Enzymes like DNA methyltransferases (DNMTs), lysine acetyltransferases (KATs), and lysine methyltransferases (KMTs) are responsible for these modifications, while "erasers" remove them to maintain cellular homeostasis. Cancer is often characterized by dysregulated epigenetic machinery, making these enzymes and their inhibitors promising targets for cancer treatment. Historically, chemotherapeutics have targeted the epigenome, with nucleotide analogues being widely used. Recent studies have identified overexpression of DNMTs, histone deacetylases (HDACs), and other epigenetic enzymes in cancer cells. Hyperactivity of these enzymes is linked to various types of cancer, and their inhibition can enhance the effectiveness of chemotherapeutics. For example, the epigenetic silencing of SALL2 confers tamoxifen resistance in breast cancer, which can be overcome by inhibiting the histone methyltransferase EZH2. The article highlights the development of inhibitors for DNA methyltransferases, HDACs, and other epigenetic enzymes, many of which are already approved or in advanced clinical trials. Natural compounds are also being explored for their potential to modulate epigenetic enzymes, either alone or in combination with chemotherapeutics to reduce toxicity. Additionally, epigenetic modifications may serve as diagnostic markers for cancer progression and prognosis. The authors acknowledge support from various institutions and declare no conflict of interest.