Two main oncogenic pathways have been identified in the pathogenesis of VSCC: (1) an HPV-dependent pathway that starts with infection with hrHPV and (2) an HPV-independent pathway that is associated with chronic inflammation (e.g., lichen sclerosus) with either wildtype p53 or mutated p53 [36,37,38]. The gene discussed is TP53; the disease is lichen sclerosus et atrophicus.