Benign nevi lesions harbored BRAFV600E mutations, while intermediate lesions were enriched in NRAS and BRAFV600E mutations and additional driver mutations; intermediate lesions and melanomas in situ harbored TERT promoter mutations, while biallelic CDKN2A inactivation, as well as PTEN and TP53 mutations, emerged only in advanced melanomas [34]. This evidence concerns the gene CDKN2A and melanoma.