Increasing evidence demonstrates that there was a consistent relationship between certain genetic variants (such as the tumor protein 53 (TP53) Arg72Pro polymorphism) and cervical cancer, most likely modulated by the presence of high-risk HPV during progression from squamous intraepithelial lesions (SIL) to cervical cancer. This evidence concerns the gene TP53 and squamous cell intraepithelial neoplasia.