It was balanced between strands in sporadic skin cancers (1.02-fold); at the same time the majority of damaging mutations in GG-NER deficient XP-E and XP-C groups were attributed to the untranscribed strand (1.36 and 1.82-fold, respectively), while in GG- and TC- NER deficient XP-D and XP-A groups – to the transcribed strand (0.77-fold and 0.65-fold, respectively, Fig. 7d). This evidence concerns the gene XPC and skin cancer.