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Various cellular responses have evolved to deal with the damage inflicted in <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> by <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>, and the study of these responses in model systems has spawned the burgeoning field of <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> repair. Although we now know of many types of deleterious alterations in <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>, the approaches for studying them and the early mechanistic insights have come in large part from pioneering research on the processing of <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content>\u2010induced bipyrimidine photoproducts in bacteria. It is also notable that <jats:styled-content style=\"fixed-case\">UV<\/jats:styled-content> was one of the first <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> damaging agents for which exposure was directly linked to cancer; the sun\u2010sensitive syndrome, xeroderma pigmentosum, was the first example of a cancer\u2010prone hereditary disease involving a defect in <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> repair. 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