Our results demonstrate that the increased phosphorylation of eIF4E observed primarily in cells transfected with high‐risk E6 oncogenes (HPV16, HPV‐18, and HPV52), as well as in HPV‐positive cervical cancer cell lines (CasKi and HeLa), is mainly related to the activation of 4EBP1 and MNK1 proteins, which are downstream targets of PI3K/AKT/mTORC1 and MEK/ERK pathways, respectively. This evidence concerns the gene AKT1 and cervical cancer.