The cancer stem cell theory hypothesizes that tumors or cancers arise from mutations or epigenetic changes in normal stem cells. These mutated or genetically modified stem cells possess the properties of normal stem cells, such as the ability to self-renew, differentiate into any cell type in the body, and resist apoptosis. This is why cancer stem cells (CSCs) are so named. It is also suggested that due to the above-mentioned properties of cancer stem cells, current cancer therapies are not entirely effective (Gil et al, 2008). Despite surgery and other therapies, even if very few of these cancer stem cells survive, they can continue to act as a source of tumors, even if the therapies eliminate all visible signs of cancer. The acquisition of immortalized proliferative potential is very important. for human tumors because otherwise the tumors will not multiply or metastasize. Mutations in progenitor cells would not be transmitted too far because they have limited replication and proliferation capacity. This will limit the growth of tumors. Therefore, if there is even a very small population of cells capable of continuous proliferation, there will be a source for producing more cells for the tumor. Clonogenic analyzes have shown that although most cells in a tumor have a limited ability to proliferate, a subset of cancer cells exists in these tumors that continually proliferate and give rise to new tumors upon transplantation. Strategy to target cancer stem cells: Identification of CSC is essential for the development of better and effective therapeutic strategies. Drugs used in current therapies and treatments target not only tumor cells, but also the standard...... middle of article ...... complicates the identification of tumor suppressor gene loss ( TSG) is epigenetic changes in the gene promoter. DNA hypomethylation and histone hyperacetylation in the promoter region lead to successful DNA transcription. Therefore, any alteration in either will disrupt gene transcription. Hypermethylation of the CpG island in the TSG promoter leading to gene inactivation has been well established. Inactivation of TSGs due to promoter methylation is relatively less than that of LOH due to chromosomal recombination or gene conversion and is therefore difficult to detect. The other epigenetic change that may contribute to inactivation of TSGs is altered histone modification, such as a reduction in histone acetylation. Histone modification may or may not be dependent on methylation. of DNA and is difficult to detect compared to LOH.