The inability to repair DNA damage properly leads to various disorders and enhanced rates of tumor development. Mammals respond to chromosomal insults by activating a complex damage response pathway. These pathways regulate known responses such as cell cycle arrest and apoptosis, and have recently been shown to control additional processes including direct activation of DNA repair networks (Ref.1). Different DNA-repair pathways operate on different types of DNA lesions. NER (Nucleotide Excision Repair) is the most flexible of the DNA repair pathways considering the diversity of DNA lesions it acts upon. The most significant of these lesions are pyrimidine dimers caused by the UV component of sunlight. Other NER substrates include bulky chemical adducts, DNA intrastrand cross links, and some forms [...]