Also the fact that, in about 50% of the wild-type mucosal melanomas and particularly of vulvar and nonvulvar melanomas [24], both RAF/MEK/ERK and PI3K/AKT pathways are actually activated strongly suggests the presence of alternative mechanisms—other than activating mutations in the c-KIT, NRAS, and BRAF genes—which can lead to constitutive activation of the ERK and AKT pathways and eventually to melanomagenesis. The gene discussed is KIT; the disease is melanoma.