Although yeast lacking Rad26 and therefore deficient in TC‐NER show no growth defect under ideal conditions (van Gool et al., 1994), the long‐term importance of this system in maintaining transcriptional homeostasis and suppressing mutations is underlined by the phenotypes of human diseases caused by TC‐NER mutations, including UV‐sensitive syndrome, Xeroderma Pigmentosum and Cockayne syndrome, which is usually caused by mutations in the human orthologue of Rad26 (Lans et al., 2019). This evidence concerns the gene ERCC6 and Cockayne syndrome.