While in genome-stable tumors ectopic induction of the cGAS-STING pathway might be beneficial, as it would trigger type I IFNs and canonical NF-Kb pathway promoting apoptosis, T-cells infiltration, and NK cells killing [56] (Figure 4A,B), cGAS-STING signaling is constitutively activated in CIN tumors, and therefore the latter type of cancers have presumably found ways to circumvent downstream immune surveillance. Here, CGAS is linked to cervical squamous intraepithelial neoplasia.