Cervical cancer (CaCx) remains one of the most frequent female malignancies, causing over 300,000 deaths every year. Persistent infection with high-risk human papillomaviruses (HPV), particularly HPV16 and HPV18 strains, drives oncogenesis and tumor maintenance through continual expression of HPV oncogenes E6 and E7. A potential strategy to overcome limitations of current treatments is the development of targeted therapies that exploit alterations in gene expression in CaCx.