EDITORIALS The Conundrum Posed by Cellular Heterogeneity in

Examining the methylation patterns of gene promoters has become a powerful tool in the effort to identify and distinguish different tumor subtypes (1,2). Typically associated with tumor suppressor genes, epigenetic silencing of gene expression has been seen in several different cancers. Aberrant hypermethyl-ation has been recorded for genes that function in various aspects of cancer biology, including cell cycle regulation, tumor sup-pression, apoptosis, and metastasis. The article by Alaminos et al. (3) in this issue is a clear extension of this previous research. DNA methylation silences gene expression through the ad-dition of methyl groups to cytosine residues of CpG-rich islands present in the promoter region of genes. Whereas housekeeping genes possess CpG regions that are typically unmethylated and therefore transcriptionally active in all cell types, tissue-specific genes are unmethylated in cells actively expressing the gene