Tolerance to p53wt during melanomagenesis can be achieved through the overexpression of its negative regulator HDM2, found in 56% cases,2,3 and loss of its functional partner on the CDKN2A locus (where p14ARF resides), which occurs in some 50% of primary melanomas.4 As p53wt is maintained at such a high frequency in melanoma, we and others propose that it may be recruited to participate in the therapeutic approach.5–7. This evidence concerns the gene CDKN2A and melanoma.