Cutaneous melanoma is the most rapidly increasing malignancy in the white European population; its clinical significance is enhanced because it can affect younger individuals (1–3). The high mortality rate among melanoma patients, second to lung cancer, is related to melanoma’s resistance to therapy once the metastastic process has started (4–6). The tumor derives from epidermal melanocytes, either activated or genetically altered; thus, important precursors include activated melanocytes present within solar lentigo or forming prema- lignant lesions such as lentigo maligna (7–10). Melanoma can also arise from relatively benign or atypical nevomelanocyte lesions (7–10). Benign lesions that can nevertheless result in melanoma include congenital melanocytic nevus, nevus of Ota, nevus of Ito, and cellular blue nevus. The atypical lesions with the same possible outcome are represented by acquired dysplastic melanocytic nevus, melanocytic dysplasia on the acral or mucosal surface, spindle cell and/or atypical epithelioid melanocytic nevus (Spitz nevus), and dysplastic and/or congenital nevus spilus (7–10).