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The field of genome evolution and population genetics has for the past half of a century assumed that genomic DNA can be divided into functional and non-functional (“junk”) regions. Experimental molecular science has found little evidence for this assumption. A majority of the noncoding parts of the human genome are transcribed (1), and numerous experimental researchers have now recognized an important functional role in the so called junk DNA regions, such as syn sites, lncRNA, psudogene transcripts, antisense transcripts, microRNA, and mobile elements (2). In fact, evidence for functional constraints on noncoding genome regions has long been recognized (3). New theoretical frameworks based on less arbitrary foundations have also appeared in recent years that can coherently account for the reality of far more functional DNAs, as well as all other major known facts of evolution and population genetics (4, 5). Nonetheless, there still remains a large gap in opinions between bench scientists in experimental biology and those on the theory side in bioinformatics and population genetics. This special issue will aim to close that gap and provide a view of evidence from a perspective that all genome regions have (or can easily acquire) functionality.

Cancer is a disease of the genome. In addition to germline and somatic mutations, cancer genomes exhibit changes in DNA methylation and chromatin structure that have a substantial impact on gene expression and cellular functions. A comprehensive catalog of all types of variants in a cancer opens new and unrivaled opportunities for understanding the mechanisms of cancer onset and progression, predicting the response to therapeutics, and providing new biomarkers for diagnosis and prognosis.