text: As observed through the literature, survivin is found to be over-expressed across many tumour types. Scientists are not sure of the mechanism that causes this abnormal over-expression of survivin; however, p53 is downregulated in almost all cancers, so it is tempting to suggest that survivin over-expression is due to p53 inactivity. Wagner et al. investigated the possible molecular mechanism involved with the over expression of survivin in acute myeloid leukemia (AML). In their experiments, they did both an epigenetic and a genetic analysis of the survivin gene promoter region in AML patients and compared the observations to what was seen in peripheral blood mononuclear cells (PBMCs) that have been shown to express no survivin. Assuming that the molecular mechanism of survivin re-expression in cancerous cells is at the transcriptional level, the authors decided to look at particular parts of the promoter region of survivin in order to see what happens in cancer cells that does not happen in normal cells that causes such a high level of survivin to be expressed. With regards to an epigenetic mechanism of survivin gene regulation, the authors measured the methylation status of the survivin promoter, since it is accepted that methylation of genes plays an important role in carcinogenesis by silencing of certain genes or vice versa. The authors used methylation specific polymerase chain reaction with bisulfite sequencing methods to measure the promoter methylation status in AML and PBMCs and found unmethylated survivin promoters in both groups. This result shows that DNA methylation status is not an important regulator of survivin re-expression during leukemogenesis. However, De Carvalho et al. performed a DNA methylation screening and identified that DNA methylation of IRAK3 plays a key role in survivin up-regulation in different types of Cancer, suggesting that epigenetic mechanisms plays an indirect role on abnormal over-expression of survivin. With regard to genetic analysis of the survivin promoter region, the isolated DNA of AML and PBMCs were treated with bisulfite, and the survivin promoter region sequence was amplified out with PCR and sequenced to look for any particular genetic changes in the DNA sequence between the two groups. Three single-nucleotide polymorphisms (SNPs) were identified and were all present both in AML patients and in healthy donors. This result suggests that the occurrence of these SNPs in the promoter region of the survivin gene also appears to be of no importance to survivin expression. However, it has not been ruled out yet that there may be other possible epigenetic mechanisms that may be responsible for a high level of survivin expression observed in cancer cells and not in normal cells. For example, the acetylation profile of the survivin promoter region can also be looked at. Different cancer and tissue types may have slight or significant differences in the way survivin expression is regulated in the cell, and, thus, the methylation status or genetic differences in the survivin promoter may be observed to be different in different tissues. Thus, further experiments assessing the epigenetic and genetic profile of different tumour types must be investigated.