Approximately 50% of the SBA tumors analyzed were CIN, characterized by frequent KRAS mutation and low-level methylation [75], while the remaining SBA tumors were MSI-H and MACS, characterized by the lack of KRAS mutations and greater incidence of high-level methylation and BRAF mutations [75], implicating two molecularly distinct SBA subtypes with unique tumorigenesis pathways. The gene discussed is KRAS; the disease is cervical squamous intraepithelial neoplasia.