cGAS–STING signaling continued to surface as a mechanistic node connecting genome instability, inflammation, and cancer immunity. A Nature Aging study found that cGAS-deficient mice show premature aging phenotypes tied to LINE1 derepression and increased inflammation, placing the DNA-sensing axis in a broader link between cellular stress and age-associated tissue changes. In a complementary immune mechanism track, work on macrophage signaling identified how a tumor-promoting micropeptide can suppress macrophage cGAS–STING interferon signaling—potentially dampening innate immune activation in the tumor microenvironment. Together, the studies reinforce that manipulating innate DNA sensing can influence both systemic inflammatory outcomes and localized anti-tumor immunity.