In summary, our study proposes that the activation of the EGFR/PI3K/AKT1/NRF2 pathway by HPV16 E7 leads to PIR/NF-κB activation in tumor oral epithelial cells, resulting in an increased cell migration, with the possibility remaining that this mechanism is involved in other epithelial cell models (Figure 7). The gene discussed is AKT1; the disease is neoplasm.