Research examining the effects of upstream targeting of cGAS is needed.75,76 Recent reports have shown that cGAMP, a product of cGAS activation, can activate DNA damage response signaling that is independent of canonical IFN pathway activity, and can induce noncanonical inflammasome pathways.75,76 In murine colon cancer models cGAS deficiency has been associated with development of colon tumors, whereas STING and type I IFN receptors knockouts show no significant increase in colon tumor rates.77 These results suggest cGAS as having STING-independent and cancer-relevant activities. The gene discussed is CGAS; the disease is malignant colon neoplasm.