The previously reported p16Ink4a expression in nevi, the benign counterpart of melanoma, and in malignant melanoma (Figure 1D) represents a tumor suppressor mechanism that, at later stages of melanoma progression, is bypassed by activating mutations (Michaloglou et al. 2005; Mooi and Peeper 2006). The gene discussed is CDKN2A; the disease is neoplasm.