In normal physiological conditions, TREX1 forms relatively lower fluidic external condensate shell surrounding the cGAS/DNA core; thus, due to the reduced access to DNA interior, its activity is remarkably mitigated, while in pathologic conditions (e.g., Aicardi–Goutières syndrome), the TREX1 mutation E198K leads to the formation of more dynamic TREX1/cGAS/DNA co-condensates driving internal DNA degradation, and ultimately suppresses STING signaling [84]. The gene discussed is CGAS; the disease is Aicardi-Goutieres syndrome.