This effect, which again is mediated by E6 or E7 capability of activating the ERK1/2 and PI3K/AKT signaling pathways, leads to an increase in VEGF-mediated tumor angiogenesis (Figure 3), this being particularly evident during H-SIL evolution into invasive SCC [205,206,207]. The gene discussed is AKT1; the disease is neoplasm.