BRAF and melanoma: The deletion, mutation, or silencing of CDKN2A disables p16 in most models of melanoma.9 Nevi with histopathological dysplasia show recurrent loss of heterozygosity of CDKN2A and TP53 loci.12 Moreover, BRAF activation may cooperate with PTEN loss to drive melanoma development.11 Although the prognosis of metastatic melanoma has been greatly improved by targeted and immune therapies, novel biomarkers are still needed to design more efficient diagnostic and therapeutic strategies.