This is because tumor cells in advanced cancers have adapted to cope with the CIN-induced chronic activation of the cGAS–STING–IFN-I pathway by re-wiring the STING downstream signaling away from IFN-I induction so that IFN-I-mediated immune stimulation is lost [48,49]. Here, STING1 is linked to cervical squamous intraepithelial neoplasia.