Even though gene targeted Trex1−/− mice did not have an increase in either mutation rate or incidence of cancer [41], depletion, silencing, or pharmacological inhibition of TREX1 in cancer cell lines or tumor mouse models stimulated the cGAS-STING immune activation, increased the downstream interferon-mediated signaling, and inhibited tumor growth [43–45, 52, 116, 117]. The gene discussed is TREX1; the disease is neoplasm.