We determined (i) p53 immunoreactivity and the proliferation marker Ki-67 to identify VSCCs arising in the setting of lichen sclerosus et atrophicus [23]; (ii) high risk HPV and p16INK4a (a marker of HPV-transforming activity) to identify VSCCs driven by viral infection [24]. This evidence concerns the gene CDKN2A and lichen sclerosus et atrophicus.