The cancer stem cell theory hypothesizes that tumors or cancers result from mutations or epigenetic changes in normal stem cells. These mutated or genetically altered stem cells possess the properties of normal stem cells such as the ability to self-renew, differentiate into any type of body cell, and resist apoptosis. Therefore, cancer stem cells (CSCs) are called that. It is also suggested that, due to the above-mentioned properties of cancer stem cells, current cancer therapies are not entirely successful (Gil et al, 2008). Despite surgery and other therapies, even if very few of these cancer stem cells survive, they can continue to serve as a source for more 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 tumors will not increase in number or metastasize. Mutations in progenitor cells would not be passed down too far as they have limited capacity to replicate and proliferate. Therefore, the growth of tumors will be limited. So, if there is even a very small population of cells with the ability to continuously proliferate, there will be a source for producing more cells for the tumor. Clonogenic assays have shown that, although most cells in a tumor have a limited ability to proliferate, in these tumors there is a subset of tumor cells that continually proliferate and give rise to new tumors during 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 norm… half of the article… implies that identifying tumor suppressor gene (TSG) loss is epigenetic changes in the promoter of the gene. DNA hypomethylation and histone hyperacetylation in the promoter region lead to proper DNA transcription. Therefore, any alteration in either will disrupt transcription of the gene. CpG island hypermethylation in the TSG promoter leading to gene inactivation has been well established. Inactivation of TSGs due to promoter methylation is relatively minor compared to LOH due to chromosomal recombination or gene conversion and therefore difficult to detect. The other epigenetic change that may contribute to the inactivation of TSGs are alterations in histone modification such as reduced histone acetylation. Histone modification may or may not depend on DNA methylation and is difficult to detect compared to LOH.