Many studies have previously reported the ability of the HPV-16 E6/E7 oncoproteins to disrupt the normal process of differentiation of human foreskin keratinocytes [21] by targeting key tumour suppressors, such as p53 [22] and pRb [23], resulting in increased levels of cell survival proteins, such as Akt [24], and disruption of the cell cycle [25]. This evidence concerns the gene AKT1 and neoplasm.