Melanoma is a rare but aggressive malignant cancer that originates from melanocytes. These melanocytes are cells found in the basal layer of the epidermis that produce melanin under the control of melanocyte-stimulating hormone. Despite the fact that melanoma represents only a small number of all skin cancers, it is the cause of more than 50% of cancer-related deaths. The high metastatic qualities and death rate, and also its prevalence among people of younger ages have caused melanoma to become a highly researched malignant cancer. Epigenetic modifications are suspected to influence the emergence of many types of cancer-related diseases, and are also suspected to have a role in the development of melanoma. In the last few years, chemical alterations in the genome have become more evident, and these alterations can be critical in the development of malignancy. This alteration process is referred to as epigenetics (Patino et al. 2008). Epigenetics is the term used to refer to stable changes in DNA that affect gene expression but do not involve changes in the underlying nucleotide sequence of the organism (Patino et al. 2008). The mechanisms by which epigenetics occur involve hypo- and hypermethylation of DNA, histone modifications by acetylation, methylation, and phosphorylation, and posttranslational modifications which include RNA silencing. These modifications can cause different expression patterns to occur, which can result in alterations to cells. Some of these alterations could result in the formation of cancerous cells or various other dangerous changes in cell function, among many other outcomes when paired together. Cancerous cells are not formed from just one change. Role of cytosine methylation in melanoma In epigenetic alterations in cancer, DNA methylation is the most studied, although it is not the only alteration that can occur. DNA methylation is a covalent modification of DNA where a methyl group is added to the C-5 position of cytosine by DNA-methyltransferases. This occurs mostly at the cytosine-phosphate-guanine dinucleotide rich regions, known as CpG islands, and are located particularly in the promoter regions of genes in the human genome (Patino et al. 2008). These promoter regions are methylated in certain ways or can be completely unmethylated. However, in an altered methylation of the CpG islands (generally where the methylation pattern is inverted), transcription can be altered which can lead to cancer. This is due to chromosomes being highly condensed, preventing RNA polymerase and other transcription factors from recognizing and binding to the DNA. This