The symptom of XP reflects a deficiency of the “nucleotide excision repair” pathway in the maintenance of the genome stability in human skin (Marteijn et al., 2014), and could be used as a model of accelerated photoaging, emphasizing a putative role of XPC and DDB1. In contrast, no gene in the “proteasome” pathway was directly linked with aging, although deeper investigation of this pathway is of interest. This evidence concerns the gene DDB1 and xeroderma pigmentosum.