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Various attempts have been made to correlate the genetic alterations observed in Spitz tumors with histopathology findings in hematoxylineosin staining,50 starting with the suggestion that HRAS mutations activate the PI3K/AKT/mTOR pathway more vigorously than BRAF or NRAS mutations and, therefore, induce larger, less pigmented tumor cells than those seen in common or congenital nevi.37 While these correlations are not always easy to evaluate, we know, for example, that HRAS mutations are associated with the following: desmoplasia

Given the absence of demonstrated abnormalities in fibril morphology or collagen synthesis, this mechanism may be the most plausible

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