The combination of increased DNA repair, together with reduced oxidative stress in the presence of 1,25(OH)2D3, may explain the higher burden of non-melanoma skin cancers observed in mice with knockout of the vitamin D receptor after chemical or chronic UV treatments [72,73] and the reduced skin cancers reported in mice exposed to long-term UV but treated topically with 1,25(OH)2D3 [51]. This evidence concerns the gene VDR and non-melanoma skin carcinoma.