DNA polymerase eta (POLH) consists of 713 amino acids and can bypass thymidine-thymidine dimers, correctly adding two dAMPs opposite to the lesion. Mutations in the POLH gene result in the loss of this bypass activity and account for the XP variant phenotype (XPV) in human xeroderma pigmentosum disorder patients. POLH can carry out TLS past various UV and chemically induced lesions via two steps: (a) preferential incorporation of correct bases opposite to the lesion (b) conditional elongation only at the sites where such correct bases are inserted (Masutani et al. 1999, Masutani et al. 2000).