Loss of function alterations in the cyclin dependent kinase inhibitor 2A (CDKN2A) locus are present in 25–35% of melanoma with a higher frequency in patients with a strong family history of melanoma, in comparison to those with sporadic melanoma, and are involved in the genesis of malignant cutaneous melanoma by generally occurring at the stage of dysplastic nevus [2,16,21,22]. This evidence concerns the gene CDKN2A and dysplastic nevus.