FGFR2 and neoplasm: The exact tumor genesis also has not been fully clarified.13,14 A multi-factorial process likely comprises immune suppression, UV damage to the skin (also virus-negative), and virus involvement.6 Virus-negative MCC also differs from virus-positive MCC, with a considerably higher mutation burden [e.g., p53, NOTch, neurofibromin 1 (NF1), fibroblast growth factor receptor 2 (FGFR2), phosphoinositide 3-kinase/AKT serine/threonine kinase (PI3K/AKT)], probably due to increased UV exposure.15–18 Immunocompromisation also promotes MCC.