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A major implication of our mutation rate study is that highly expressed genes are preferentially protected from DNA damage; however mechanisms such as transcription-coupled repair do not explain our observations. There are early indications that similar mechanisms operate in cancer. DNA damage repair is traditionally studied from a molecular perspective: we have initiated collaborations with the Mammalian Genetics Group to examine this phenomenon from a genomic viewpoint also. This will dramatically improve understanding of how DNA damage repair operates on a genome-wide scale.