Given the multiple roles played by the cGAS-STING axis in not only the recognition of a variety of pathogens but also the induction of antitumor immunity and tumor cell-specific apoptosis, the inhibition of cGAS-STING signaling by Meq may contribute to Meq-induced tumorigenesis in addition to establishment of persistent infection. The gene discussed is STING1; the disease is neoplasm.