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. The gene discussed is NFKB1; the disease is cancer.