The experimental animal model studies demonstrate that some cancer genes (such as BRAF, NRAS, MITF, TP53, P16/CDKN2A, BAP1, PTEN, C‐KIT, etc) can drive naevus formation and/or progression to melanoma in various combinations, while sequencing studies of human melanomas emphasize the genetic heterogeneity of the disease with potential for reclassification based on the genetic phenotype in the future. The gene discussed is CDKN2A; the disease is melanoma.