“…AM differs from the other melanoma forms in the biological profile causing specific genetic/immunohistochemical features and related behaviors [ 8 , 9 , 10 , 11 , 12 ]: first, it is a non-UV-related tumor arising from the epithelium-associated melanocytes; second, it shows the early onset of major chromosomal rearrangements with gene copy number changes and multiple high-level amplifications (e.g., driver mutations in GNAQ, NF1, KIT TP53, PTEN, or RB1 genes, versus BRAF and NRAS of superficial spreading and nodular melanoma) [ 13 ]; third, it exhibits specific molecular findings (e.g., CCND1 overexpression , AURKA , and TERT) [ 14 ]; fourth, it is characterized by a rapid evolution and ability to metastasize and, thus, a poor prognosis [ 15 , 16 , 17 ]. This said, AM is also known for having a late diagnosis compared with other forms: the more reported underlying hypothesis emphasize the patients’ (and/or physicians’) reticence in examining this area and the difficulty of the differential diagnosis with acral nevi -with reported rates of misdiagnosis of 20%—despite dermoscopic examination [ 18 , 19 , 20 , 21 ]. Dermoscopy is nowadays the most common technique for non-invasive imaging in dermatology, able to provide a “radiography” of pigmented skin lesions through a polarized light source that reaches the dermal–epidermal junction [ 22 ].…”