In contrast to the RelA-mediated classical NF-κB pathway, the RelB-driven non-classical NF-κB pathway inhibits the release of type I IFNs.642 Chronic stimulation of the cGAS-STING by CIN tumors causes a dominance of the non-classical NF-κB pathway in tumor cells, which in turn facilitates tumor metastasis through STING activation.13 A recent article also reported that tumor cells promote metastasis by activating the endoplasmic reticulum stress response downstream of STING.12 This evidence concerns the gene CGAS and neoplasm.