The detection of predominant TrkAIII splicing in advanced stage and recurrent stage IV MCPyV positive MCCs also adds to reports that predominant TrkAIII splicing associates with advanced stage metastatic disease and post-therapeutic relapse in neuroblastoma, characterizes a subset of advanced stage EGFR and EGFRvIII negative glioblastomas and has been detected in metastatic melanoma [19–25], supporting the hypothesis that predominant alternative TrkAIII splicing and intracellular TrkAIII activation represents a novel oncogenic mechanism and potential target in a subset of MCPyV positive MCCs. This evidence concerns the gene EGFR and glioblastoma.