Several important reports revealed a novel strategy on how high-risk HPVs can abolish the innate immune response in their genuine host cells in cervical cancer were demonstrated, in which an epigenetic silencing of type I IFN after HPV16 oncogene expression and that IFN-κ expression is suppressed by de novo methylation within a CpG-rich area near the transcriptional start site, IFN-κ being the only keratinocyte-specific IFN involved in innate immunity. The gene discussed is IFNA1; the disease is cervical cancer.