The growth mechanism of VS is well known to be associated with abnormalities in the Merlin protein [34], a tumor suppressor gene that activates receptor tyrosine kinases, such as ErbB, PDGF, VEGF, and C-kit, and activates the downstream pathways PI3K/AKT/mTOR and MEK-ERK1/2. This evidence concerns the gene EGFR and neoplasm.