Since blocking IFN signaling increases metastasis but not primary tumor growth in MMTV-PyMT mice [48] and forced RHAMM expression activates cGAS-STING in a BRCA1 mouse model of breast cancer susceptibility [14], we assessed if Rhamm−/− cells have an aberrant cGAS-STING-IFN signaling, which provides a survival advantage in lung tissue. Here, STING1 is linked to neoplasm.