In contrast with acquired nevi, congenital nevi are usually characterized by mutations in the NRAS gene, very often at codon 61.3,4 Exposure to sunlight is one of the most important factors although not the only one in the pathogenesis of melanoma,57 with more genetic aberrations being observed in tumors that develop as a result of intense, prolonged exposure to sunlight.813 On the other hand, melanomas that may have little or no association with sunlight (e.g., acral melanoma) have a low mutational burden.1315 UV-A radiation is less carcinogenic than UV-B radiation: the former induces oxidation of guanine in DNA, whereas the latter generates oncogenic cyclobutane dimers.16,17 Decades of examining melanomas through an optical microscope have revealed the broad morphological variety of these tumors, which can present as various lesions, for example, superficial spreading melanoma, nodular melanoma, spitzoid melanoma, and acral melanoma
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Despite the fact that the ferroptosis triggered by these pathogens has not been validated in skin tissues, these studies bring new insights into the research of their respective pathogenesis and therapeutic targets (Figure 4)
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