“…Xeroderma Pigmentosum (XP), Cockayne syndrome (CS) and Ataxia telangiectasia (AT) are genetic diseases resulting from rare autosomal recessive pathologies involving DNA repair enzymes that are deficient due to inactivating mutation in their genes [9,10,11]. These diseases are characterized at the level of the skin by extreme sensitivity to sunlight, resulting in sunburn, pigmentation changes, an early onset of the appearance of skin aging signs and a greatly elevated incidence of skin cancers in particular for XP disorder [12]. These changes can be explained by long lasting DNA damages that induces prolonged cellular inflammation through the activation of the NF-κB pathway [2,13,14,15,16] and an acquired immune deficiency [17] as well as rapid accumulation of mutation leading to cell apoptosis, senescence and cell tumorigenesis [18,19,20,21].…”