GTF2H1 and melanoma: Accordingly, repair of cyclobutane pyrimidine dimers (CPD) as a predominant type of UV-induced DNA lesion as well as cisplatin-induced primary DNA mono-adducts and subsequently formed intrastrand crosslinks, both of which constitute NER substrates, was substantially delayed upon depletion of MITF or GTF2H1 in primary melanocytes and melanoma cells, respectively (Fig. 3c, and Supplementary Figures 4b-d) [39].