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Protein coding genes account for only 1 percent of the DNA sequences in the human genome. While the remaining 99 percent remains largely uncharacterized, these vast stretches of “non-coding” DNA contain instructions for regulating gene activity in the human body’s 200+ cell types. These sequences interact with regulatory factors such as transcription factors, chromatin regulators, and are regulated by a plethora of histone modifications and DNA methylation. Together these proteins and modifications constitute the epigenome: a layer of control mechanisms and information atop the genome that defines the gene regulatory program of every cell.

The ӳ����ý's Epigenomics Program seeks to decode the human epigenome and enable researchers to more precisely interpret disease risk, including the genetic and lifestyle differences between individuals that cause epigenomic dysfunction that ultimately lead to diseases. Based on this knowledge, the program works to develop diagnostics and therapeutics for cancer and developmental, metabolic, psychiatric diseases. 

Maps of these elements and their interactions provide critical insights into human genome regulation, in turn revealing new information about cell function, identity, and proliferation. The vast majority of the genetic variants that confer risk of common diseases — e.g., cardiovascular disease, type 2 diabetes, obesity — are noncoding, and frequently coincide with these regulatory elements. Further, methylation of the DNA, which results from development, aging and exposure throughout life, alters the function of regulatory elements and genes.