This suggests that activating cGAS-STING pathway may be an effective modality for anti-HBV and holds great promise for the future treatment of chronic hepatitis B. Although STE-boosted cGAS-STING signalling potently curtailed HBV replication in our model, sustained hyper-activation of this axis could generate high systemic levels of IFN-β and IL-18, raising concerns about cytokinaemia-related adverse events. The gene discussed is IFNB1; the disease is chronic hepatitis B virus infection.