While activation of cGAS/STING normally induces cell death due to interferon/TLR/STAT1, CIN-induced STING signaling resulted in enhanced survival and proliferation due to non-canonical NFKB (RelB) (Bakhoum et al., 2018) as well as IL-6/JAK2/STAT3 signaling (Hong et al., 2022). This evidence concerns the gene STAT1 and cervical squamous intraepithelial neoplasia.