CGAS and neoplasm: Our study shows that the T-cell-dependent anti-tumor effect of CTX critically involves the cGAS–STING–IFN-I axis, the IFN-I response, and the STING-independent cGAS function of host myeloid cells, which supports the deployment of CTX in treating advanced solid tumors by bypassing the often-failed IFN-I production by tumor cells due to a chronic activation of the intrinsic cGAS–STING caused by chromosomal instability.