EBV-positive tumors are characterized by DNA hypermethylation, frequent phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) mutations, and programmed cell death ligand 1 (PD-L1)/programmed cell death ligand 2 (PD-L2)/Janus kinase 2 (JAK2) overexpression; MSI tumors have high mutation and DNA methylation rates; CIN tumors contain chromosomal alterations affecting mainly tyrosine kinase receptors; and finally, GS tumors are chromosomally stable and have a high frequency of cadherin 1 (CDH1) and Ras homolog family member A (RHOA) mutations [Table 1][4]. This evidence concerns the gene RHOA and cervical squamous intraepithelial neoplasia.