In particular, we used two well-characterized models harbouring constitutively activated PI3K signaling in melanocytes downstream (i) mutated Nras (Tyr:NrasQ61K;Ink4a/Arf−/−) [51] or (ii) Pten loss, the latter in a melanoma-prone background of constitutively active BRAFV600E (Tyr::CreERT2;BrafCA;Ptenfl/fl) [52]. This evidence concerns the gene CDKN2A and melanoma.