Interestingly, the annealing helicase SMARCAL1—which catalyses replication fork reversal and Holliday junction migration to maintain genome stability during replication [67–69], was shown to suppress cGAS-STING signalling in cancer cells by limiting endogenous DNA damage [70], while the structure-specific helicase BLM—which also mediates Holliday junction resolution [71], has conversely been shown to promote [45] or prevent [72] the accumulation of immunogenic DNA fragments in the cytosol, suggesting a double-edged sword feature of DNA helicases. Here, CGAS is linked to cancer.