This is followed by the adenoma-to-carcinoma transition (in CIN) through sequential genetic mutations in oncogenes (e.g., KRAS, PIK3CA, PTEN, or EGFR/ERBB family members) and/or tumor suppressor genes (e.g., TP53, SMAD4, BAX) [12,13]. This evidence concerns the gene EGFR and cervical squamous intraepithelial neoplasia.